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Quantitative Magnetic Resonance Imaging in Optic Neuritis Quantitative magnetic resonance imaging in optic neuritis Simon James Hickman A thesis submitted to the University of London for the degree of Doctor of Philosophy 2004 NMR Research Unit Department of Neuroinflammation Institute of Neurology University College London Queen Square London WC1N3BG United Kingdom UMI Number: U602525 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a complete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. Dissertation Publishing UMI U602525 Published by ProQuest LLC 2014. Copyright in the Dissertation held by the Author. Microform Edition © ProQuest LLC. All rights reserved. This work is protected against unauthorized copying under Title 17, United States Code. ProQuest LLC 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 48106-1346 i Abstract The major event in relapsing remitting multiple sclerosis (MS) is the acute relapse. The majority of patients with MS present with such an event. Most early relapses are followed by complete or near complete recovery, however partial recovery or significant disability can result from an individual relapse. Study of relapses in vivo is therefore desirable. Magnetic resonance imaging (MRI) is very sensitive at detecting MS lesions. Unfortunately, in the brain and spinal cord, it has been difficult to reliably identify the lesion that is responsible for the symptoms of an individual relapse and most new brain lesions which are apparent on MRI are clinically silent. Optic neuritis provides an attractive model to study the effects of relapses in MS. Optic neuritis is a frequent manifestation of MS and has been regarded as a forme fruste of the disease. The natural history of acute optic neuritis mirrors that of an acute MS relapse elsewhere in the central nervous system (CNS) and the response to corticosteroid therapy is the same. Visual function can be measured accurately in a rater-independent fashion and it is possible to measure the latency and amplitude of the visual evoked potential (VEP) which gives information about the integrity of the visual conducting pathways. Developments in imaging technology and application now means that, potentially more pathologically specific imaging sequences can be applied to the study of the optic nerves. This thesis will investigate the application of these new imaging techniques, along with clinical and VEP measures, to the study of optic neuritis in order to gain new insights into the effect of individual lesions on structure and function in the CNS in the short- and long-term. Declaration Patient recruitment and examinations for the studies in Chapter 3.1 and 3.2 were performed by Dr. Peter Brex in London and Dr. Charlotte Brierley in Cambridge. The images were reported by Dr. Ivan Moseley. Statistical advice was provided by Dr. Martin King. Patient recruitment and examinations for the study in Chapter 3.3 were performed by Dr. R. Kapoor, Dr. G.T. Plant, Dr. S.J. Jones, Dr. A. Brusa, Dr. A. Gass, Dr. C.P. Hawkins, Dr. R. Page, Prof. N.W. Wood, Prof. D.A.S. Compston, Dr. I.F. Moseley, Prof. W.I. McDonald, Mr. D.G. MacManus, and Mrs. M. Galton. Statistical analysis was performed by Dr. Daniel Altmann. In Chapter 4 visual evoked potentials were recorded and analysed by Dr. Stephen Jones. The conventional MRIs were reported by Dr. Katherine Miszkiel. Statistical analysis was performed by Dr. Daniel Altmann. Acknowledgements I would first like to thank all the willing participants, both patients and controls, who volunteered to spend endless hours in the imager and have numerous clinical tests. Without them all this would not have been possible. Dr. Peter Brex and our collaborators in Cambridge: Dr. Charlotte Brierley, Prof. Neil Scolding and Prof. Alastair Compston provided patients for the studies in Chapter 3, which enabled me to get started and develop the segmentation methodology for optic nerve atrophy measurement. Patient recruitment for the studies in Chapter 4 was carried out in the Neuro- Ophthalmology clinic at Moorfield’s Eye Hospital. I am indebted to Michelle Peppiatt for organising the optic neuritis clinic and to Dr. Gordon Plant for kindling my interest in the field of Neuro-Ophthalmology. I would like to thank the radiographers David MacManus, Andrew Lowe, Ros Gordon and Chris Benton for putting up with me and for imaging all the subjects. Reporting of the images was performed by Dr. Ivan Moseley and Dr. Katherine Miszkiel. Dr. Steve Jones did all the hard work performing and analysing the visual evoked potential experiments. His was also the voice of reason making sure that I did not get too carried away with outlandish conclusions. The support of the fellows’ room kept me going; firstly Drs. Jackie Foong, Manny Bagary and Stefania Bruno and latterly Drs. Declan Chard, Ahmed Toosy, Gordon Ingle, Gerard Davies, Waqar Rashid, Olga Ciccarelli, Tony Traboulsee, Catherine Dalton and Jaume Sastre-Garriga. This work would not have been possible without the technical support of the Physicists, particularly Drs. Geoff Parker and Claudia Wheeler-Kingshott, and Prof. Gareth Barker who also acted as my secondary supervisor, providing sage advice. Statistical advice and support was also vital and I am indebted to Drs. Martin King and Daniel Altmann for getting me to think more clearly about the data. Profs. Alan Thompson and David Miller conceived the idea for this project and secured the funding to enable it to proceed. Prof. Miller also acted as my principal supervisor. He displayed a good mix of gentle support when it was needed and a firm hand to make sure that I kept the writing-up going to publish the data and produce this work. I would like to thank him especially for his help. The NMR Research Unit is supported by the Multiple Sclerosis Society of Great Britain and Northern Ireland. Their financial support keeps the Unit going. I was supported by a project grant from The Wellcome Trust. I am indebted to these two organisations for enabling me to complete this PhD. Lastly I would like to thank my wife Rosemary and children Stephanie and Alistair for putting up with me for the last few years and for always being there. V Publications associated with this thesis Hickman SJ, Brex PA, Brierley CMH, Silver NC, Barker GJ, Scolding NJ, Compston DAS, Moseley IF, Plant GT, Miller DH. Detection of optic nerve atrophy following a single episode of unilateral optic neuritis by MRI using a fat saturated short echo fast FLAIR sequence. Neuroradiology 2001;43:123-128. Hickman SJ, Brierley CMH, Brex PA, MacManus DG, Scolding NJ, Compston DAS, Miller DH. Continuing optic nerve atrophy following optic neuritis: A serial MRI study. Mult Scler 2002;8:339-342. Hickman SJ, Dalton CM, Miller DH, Plant GT. Management of acute optic neuritis. Lancet 2002;360:1953-1962. Hickman S J, Kapoor R, Jones S J, Altmann DR, Plant GT, Miller DH. Corticosteroids do not prevent optic nerve atrophy following optic neuritis. J Neurol Neurosurg Psychiatry 2003;74:1139-1141. Hickman SJ, Toosy AT, Jones SJ, Altmann DR, Miszkiel KA, MacManus DG, Barker GJ, Plant GT, Thompson AJ, Miller DH. Serial magnetization transfer imaging in acute optic neuritis. Brain 2004;127:692-700. Hickman SJ, Toosy AT, Miszkiel KA, Jones SJ, Altmann DR, MacManus DG, Plant GT, Thompson AJ, Miller DH. Visual recovery following acute optic neuritis: A clinical, electrophysiological and magnetic resonance imaging study. J Neurol 2004, in press. Table of Contents Abstract i Declaration ii Acknowledgements iii Publications associated with this thesis v Table of contents vi Abbreviations xi List of figures xv List of tables xviii Chapter 1 Optic Neuritis 1 1.1 Anatomy and physiology of the optic nerve 1 1.1.1 Gross anatomy 1 1.1.2 Optic nerve head 1 1.1.3 Intraorbital optic nerve 1 1.1.4 Intracanalicular optic nerve 2 1.1.5 Intracranial optic nerve 3 1.1.6 Optic chiasm 3 1.1.7 Optic nerve histology and physiology 4 1.2 Optic Neuritis 6 1.2.1 Presentation of optic neuritis 6 1.2.2 Fellow eye involvement 8 1.2.3 Recovery 9 1.2.4 Differential diagnosis 10 1.2.5 Investigations 13 1.2.6 Treatment of optic neuritis 15 (i) Recommendations for management 18 (ii) Management of bilateral optic neuritis 20 (iii) Management of childhood optic neuritis 20 1.2.7 Late outcome and the risk of recurrence of optic neuritis 20 1.2.8 The association between optic neuritis and multiple sclerosis 21 vii 1.2.9 Treatments to delay the onset of multiple sclerosis after optic neuritis 24 (i) Recommendations for management 26 1.2.10 Optic neuritis pathology 27 1.2.11 The pathophysiology of optic neuritis 34 (i) Phosphenes 38 (ii) Uhthoff s phenomenon 38 (iii) Pulfrich’s phenomenon 38 (iv) Fading of vision 39 Chapter 2 Magnetic Resonance Imaging in Optic Neuritis 46 2.1 Theory of Magnetic Resonance Imaging 46 2.1.1 Ti and T 2 relaxation 48 2.1.2 The spin echo pulse sequence 48 2.1.3 Generating the image in space 52 2.1.4 The slice-select gradient 52 2.1.5 The frequency-encoding gradient 53 2.1.6 The phase-encoding gradient 53 2.1.7 Image processing 54 2.2 Optic nerve imaging 55 2.2.1 Artefact 56 (i) Chemical shift artifacts 56 (ii) Motion artifacts 57 (iii) Susceptibility artifacts 57 2.3 Magnetic resonance imaging in optic neuritis 58 2.3.1 Short tau inversion recovery imaging 58 2.3.2 Chemical shift imaging 60 2.3.3 Frequency selective fat saturation 60 2.3.4 Fat saturated fast spin
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