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English Choose a language for shopping. Amazon Music Stream millions of songs. Amazon Drive Cloud storage from Amazon. Alexa Actionable Analytics for the Web. Secondly, with my physiological background I have a deep interest in mechanism and optic neuritis provides an ideal model in which to explore it, not only for itself, but for the light it sheds on multiple sclerosis, of which it is so often a part.
I shall devote the remainder of this lecture to discussing some of the clinical issues surrounding optic neuritis, how the study of it illuminates the mechanism of relapse and remission in multiple sclerosis, and finally whether and how it should be treated. Optic neuritis is a source of considerable alarm for the sufferer, who may wake in the morning, having gone to bed normal to find that she for it is more often a woman than a man is unable to see clearly. The vision usually deteriorates further over the next few days, often accompanied by discomfort which may have preceded it.
By the time the physician first sees the patient, the anxious individual has a number of questions: What is the matter? Will I get better? Will the symptoms recur? Will I develop multiple sclerosis? Should I be treated? The diagnosis of optic neuritis is relatively easy and I need not rehearse it to this audience.
It is, however, difficult for us as physicians — I use the term generically, as Johnson did, and so include ophthalmologists — to appreciate what the experience of the disease is like for the sufferer. This situation has changed as a result of the paintings and writings of Peter MacKarell, a lecturer in fine art at Goldsmiths College of the University of London. He had a series of episodes of optic neuritis and subsequently developed multiple sclerosis. The next day, upon waking I discovered that there was over the central zone of vision of my right eye, what seemed like a grey asbestos mat In three days all response was lost.
The feeling was like peering through a thick screen of dirty net curtains or butter muslin It seemed to shine like an astronomic phenomenon in interstellar space.
Later I began to notice that my appreciation of space was wayward To my amazement I became aware that as I lay in bed that the metal curtain rail which surrounded the bed-space seemed to wobble in and out of the background of the opposite wall. Surfaces appeared liquid rather than solid He made a virtually full recovery, but later had a second episode.
He was at the Royal Ballet with his daughter for a performance of Cinderella. Through the newly affected eye the Ugly Sisters dressed for the ball. I began to really enjoy the iridescence for it was like having a neoimpressionist painting — a Seurat or Signac — magically dancing about in the visual field of the affected eye. It is as if the coherence and integration of vision including the admission of light was about to fragment and fade like a cinematic device.
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There have been many reports of the prognosis for vision in optic neuritis. No factors have been consistently shown to be predictive of a poor outcome. In a subsequent study 21 in which MRI was performed both at presentation and later, these correlations were found to apply to the characteristics of the late lesion, but not to those at presentation. This question is being asked with increasing frequency as patients become more knowledgeable. That multiple sclerosis may subsequently develop after optic neuritis is a fact recorded in history long before the disease itself was described.
On my arrival I found him dead Shortly after the funeral I was obliged to have my letters read to me, and their answers written for me, as my eyes were so attacked that when fixed upon minute objects indistinctness of vision was the consequence: Soon after, I went to Ireland, and without anything having been done to my Eyes, they completely recovered their strength and distinctness of vision October 17, To my surprise in Venice I one day found a torpor or indistinctness of feeling about the Temple of my left Eye. At Florence I began to suffer from a confusion of sight: Each eye had its separate visions.
Kissock supposed bile to be the cause: I was twice blooded from the temple by leeches; — purges were administered; One Vomit, and twice I lost blood from the arm: I was able to go out and walk. Now a new disease began to show itself: At length about the 4th of December my strength of legs had quite left me I remained in this extreme state of weakness for about 21 days All this occurred a decade before Carswell 27 first drew then published the first depiction of the lesions of multiple sclerosis.
He was a 23 year old man who. He had, at the commencement of his illness,. McKenzie describes how he was incontinent and was developing an asymmetric weakness of the arms and dysarthria. After 3 weeks in hospital and frequent purges he began to improve. The late 19th century neurologists knew well that visual loss was an important manifestation of multiple sclerosis. As to pathology, Lumsden 32 reported that all of 35 postmortems showed optic nerve involvement. But patients want to know what the risk is for them. This is more difficult to determine than it might seem, as the figures in the table show.
Several factors are likely to contribute. Firstly, there is the selection of patients: The duration of follow up, diagnostic criteria, geographical location and race also vary, and may influence the results. Can one predict the likelihood that a patient will develop multiple sclerosis? Several risk factors have been studied, but only three have been consistently shown to be of value: The last two deserve further comment. Retinal perivenous sheathing as a risk factor was first reported by Lightman et al 48 in a prospective study.
They found a fold increase in risk after a mean of 3.
They found a fold increase in risk after a mean of 3. This book is not yet featured on Listopia. Are you an author? Jason Bradley marked it as to-read Feb 23, The question is whether one can improve on that?
Recently, Rodriguez et al 19 confirmed this observation, albeit at a rather lower level of significance, perhaps because of the retrospective nature of the study. The results of numerous investigations are highly consistent. This is much less common than acute unilateral optic neuritis. The long term follow up of the cases of Heirons and Lyle 9 already referred to 10 raised the possibility that multiple sclerosis might be less frequent than after unilateral optic neuritis. Five had developed multiple sclerosis and the remaining 14 still had isolated optic neuropathy.
The numbers are small, but the results lend some support to the suggestion that multiple sclerosis may be less frequent after bilateral than unilateral optic neuritis. However, it occurs sufficiently often for prudence to dictate a cautious prognosis. I turn now to my other interest in optic neuritis: As we have seen, recovery after optic neuritis is usual, as after acute relapses of multiple sclerosis.
Optic neuritis thus provides an excellent opportunity to investigate the mechanisms of relapse and remission. It is in the nature of clinical research that one is dependent on the chance occurrence of disease and of the patient presenting with it. Thus, one is often dependent on data from different sources to make a coherent story. It is important therefore to summarise the reasons why I think it is legitimate to use observations on optic neuritis to illuminate multiple sclerosis. Firstly, there is the frequency with which optic neuritis is indeed a part of multiple sclerosis. Secondly, there is the evidence that the characteristic pathology in both is demyelination.
This can be seen directly at postmortem in the case of optic neuritis in the course of multiple sclerosis, and can be inferred from the observation of delayed visual evoked potentials in isolated optic neuritis. Thirdly, there are close similarities in the pathology in the brain and optic nerve in multiple sclerosis. Finally, there is evidence that the inflammation is immunologically mediated at both sites. It is now appropriate to consider what we have learnt from the study of optic neuritis and multiple sclerosis about the development of symptoms and recovery in both. It has been possible to shed light on these problems by combining clinical, electrophysiological, magnetic resonance, and pathological studies.
Here there is a wide range of expertise in neurology, radiology, and physics; important collaborations have been developed with neuropathology, clinical neurophysiology, neuropsychology, and neuropsychiatry. It is well established that the areas of high signal on proton density and T2 weighted MR imaging of the brain correspond with plaques. Enhancement represents a focal breakdown of the blood-brain barrier and pathological studies of postmortem and biopsy material indicate that this breakdown is seen in association with focal inflammation.
The earliest detectable event in most lesions is a focal breakdown of the blood-brain barrier which may occur in otherwise MRI-normal white matter.
The application of short-echo time spectroscopy to new lesions indicates that demyelination begins during the active inflammatory phase, as judged by gadolinium-DTPA enhancement. Evoked potential studies within 24 hours of the onset of symptoms in optic neuritis provide evidence that demyelination is already present at this time. The serial study of such patients allows one to relate the changes in function to the changes in pathology as shown by NMR methods. A month later, enhancement had ceased in all but two of the nerves, indicating that the natural history of enhancement in acute isolated optic neuritis is similar to that of the lesions in the brain in multiple sclerosis.
The clinical features of optic neuritis pain, reduced acuity, impaired colour vision, afferent pupillary defect occurred during the enhancing—that is, the inflammatory phase. Of particular interest were the electrophysiological findings. At presentation, there was a marked reduction in the amplitude signifying conduction block in most fibres from the affected nerve. What remained of the evoked potential was, however, delayed indicating that demyelination was already established. A month later the amplitude of the evoked potential had increased indicating that conduction had been restored in many fibres.
It is well established experimentally that acute demyelination produces conduction block.
The difference in the state of the nerve at the two recording times is that there was inflammation as judged by gadolinium enhancement at the early stage when conduction block was severe , but not at the later stage. Because demyelination was present at both times, these observations suggest that the inflammatory process itself contributes to conduction block. Two questions now arise:. Recent experiments on the rat spinal cord have provided evidence that nitric oxide which is produced in abundance by macrophages, which are a prominent part of the acute lesions in multiple sclerosis has a concentration related blocking effect on demyelinated and normal fibres.
New sodium channels can be inserted into the axonal membrane in demyelinated internodal segments of central and peripheral nerve fibres. It therefore seems likely that in multiple sclerosis, as in experimental lesions, the restoration of conduction which underlies the restoration of function depends to an important extent on the development of new sodium channels in the demyelinated axons. There is evidence that remyelination occurs in the CNS and that in some lesions it may be extensive.
Subsequent shortening of the latency, 75 particularly in children, 11 suggests that remyelination may play some part in maintaining function later. To sum up, inflammation and demyelination occur early in the development of the new lesion. Both these processes contribute to the development of conduction block and therefore of symptoms. This is the mechanism of relapse. In the succeeding weeks new sodium channels are formed in the demyelinated axons. When the inflammation subsides, conduction is restored and the symptoms resolve.
This is the mechanism of remission.
The question is whether one can improve on that? A variety of forms of steroid treatment have been studied. They have consistently shown that the duration of visual impairment is shortened but that visual outcome is unchanged. A surprising finding in the first report 18 was a decreased risk of recurrence of optic neuritis in patients treated with intravenous steroids as compared with those treated with oral steroids or placebo. An even more surprising later finding was that after 2 years the risk of progression from optic neuritis to clinically definite multiple sclerosis was higher in patients treated with oral steroids than in those treated with intravenous steroids.
Inspection of the Kaplan-Meier survival curves shows that the absolute numbers of patients in the different groups at the later periods of follow up was small. It was not therefore surprising that after a further 2 years of follow up the apparent difference between the frequency of development of multiple sclerosis in the treated groups had disappeared. My policy is to treat optic neuritis with steroids when there is severe visual loss, either in bilateral optic neuritis or in unilateral optical neuritis when there is poor vision in the other eye from whatever cause.
In this way the duration of functional impairment may be shortened. I generally use intravenous steroids, because the course is quickly completed. However, as the evidence that oral steroids increase the risk of developing of multiple sclerosis is equivocal, I think that it is reasonable to use oral steroids if that is more convenient for the patient. In this saga, I suggest that we have fallen into the Johnsonian trap just as surely as Dr Lucas did.