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Mechanisms of Axon-Glial Injury of the Optic Nerve

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Mechanisms of Axon-Glial Injury of the Optic Nerve Eye (2004) 18, 1182–1187 & 2004 Nature Publishing Group All rights reserved 0950-222X/04 $30.00 www.nature.com/eye CAMBRIDGE OPHTHALMOLOGICAL SYMPOSIUM Mechanisms of A Compston axon-glial injury of the optic nerve Abstract think merely in terms of demyelination as the sole consequence of brain inflammation. Rather, The central concept underlying ideas on the symptom onset and recovery must be pathogenesis of multiple sclerosis is that understood in terms of altered structure and inflammatory events cause acute injury of function in the entire myelinated axons and myclin. The phases of symptom oligodendrocyte–axon unit. onset, recovery, persistence, and progression in multiple sclerosis can be summarized as functional impairment with intact structure due to direct effects of inflammatory Mitochondrial disease and the optic nerve mediators; demyelination and axonal injury with recovery through plasticity and Genetic factors are implicated in the aetiology of remyelination; and chronic axonal loss due to multiple sclerosis. The best characterized region failure of enduring remyelination from loss of of interest is the major histocompatibility trophic support for axons normally provided complex encoded at chromosome 6p21. by cells of the oligodendrocyte lineage. Cell Possession of the DR15 susceptibility allele in death may occur in response to a state of injury individuals with optic neuritis increases the risk from which protection would be anticipated of conversion to multiple sclerosis.1 This merely under more favourable neurobiological reflects the relationship of optic neuritis to conditions. Conversely, optimal growth factor multiple sclerosis. Potentially more revealing is environment may save cells from otherwise the identification of a multiple sclerosis-like lethal events occurring at the cell membrane. illness in women, presenting with bilateral Hence, in the context of brain inflammation, sequential optic neuropathy and later there is an inseparable interplay between developing symptoms consistent with immunological and neurobiological demyelination outside the visual system, in contributions to tissue injury. whom there are mutations of mitochondrial Department of Clinical 18, 2 Neurosciences Eye (2004) 1182–1187. doi:10.1038/sj.eye.6701561 DNA (Harding’s disease). This immediately University of Cambridge suggests a genetic basis for selective Clinical School Keywords: optic nerve; multiple sclerosis; involvement of the optic nerve in demyelinating Addenbrooke’s Hospital inflammation; demyelination; axonal injury; disease. Around 45% of individuals with Hills Road, Cambridge, UK growth factors; remyelination pathological mutations of mitochondrial DNA have clinical manifestations outside the visual Correspondence: system.3 But mitochondrial mutations are rarely A Compston Department of Introduction Clinical Neurosciences identified with systematic screening of University of Cambridge As the symptoms are immediately apparent to unselected patients, although the yield is higher Clinical School affected individuals, optic neuritis provides in patients with severe visual failure Addenbrooke’s Hospital special opportunities for clinical and complicating demyelinating disorder of the Hills Road Cambridge CB2 2QQ, UK experimental analysis of brain inflammation. central nervous system. What remains Tel: þ 44 1223 217091 The spectrum of inflammatory optic neuropathy unresolved is whether the mutation of Fax: þ 44 1223 336941 includes conditions confined to the optic nerve mitochondrial DNA in Harding’s disease E-mail: DASCompston@ and those also affecting other parts of the directs the process of brain inflammation onto aol.com central nervous system. It follows that the optic a particular siteFconstituting selective tissue nerve provides a general window on the vulnerabilityFor merely represents the Received: 4 September 2003 aetiology, mechanisms of symptom onset and chance occurrence of relatively mild multiple Accepted: 4 September recovery, and pathogenesis of inflammatory sclerosis and Leber’s hereditary optic 2003 brain disease. No longer is it appropriate to neuropathy. Axon-glial injury of the optic nerve A Compston 1183 In neuromyelitis optica (Devic’s disease), Pathogenesis of brain inflammation demyelination affects the spinal cord and optic nerve. The clinical course in multiple sclerosis is initially These sites may be affected serially and in either order. characterized by episodes with full recovery, later by Magnetic resonance imaging (MRI) does not typically attacks that leave persistent deficits and, as the frequency show lesions at other sites in the central nervous system.4 of new exacerbations eventually decreases, by the onset Pathologically, the affected areas show inflammation of secondary progression. Transition between these three with extensive necrosis and deposition of antibody and stages is usually gradual and indistinct, making for many complement.5 Patients may respond to plasma intermediate forms of the disease. This clinical course is exchange.6 However, the severe optic neuropathy the expression of focal tissue injury affecting the brain occurring in the context of neuromyelitis optica among and spinal cord and resulting from the complex interplay Caucasians is also not associated with mutations of mitochondrial DNA.7 Thus, mutations of mitochondrial of inflammation, axonal injury, demyelination, DNA evidently do not easily account for the high remyelination, astrocytosis, and tissue atrophy. frequency of optic nerve involvement. However, visual The central concept underlying ideas on the involvement in multiple sclerosis may generally be pathogenesis of multiple sclerosis is that the cascade of associated with the mitochondrial K and J haplogroups, inflammatory events that culminates in demyelination of suggesting that these serve as population markers of axons depends on the peripheral activation of T autosomal genes conferring selective tissue susceptibility lymphocytes. Activated T cells express adhesion to demyelinating disease.8 molecules on their surface and upregulate complementary molecules on the luminal surface of blood vessels, allowing them to cross the blood–brain barrier by diapedesis. Within the central nervous system, these T cells re-encounter specific antigen and set up an Clinically isolated optic neuritis inflammatory process that resembles delayed-type Optic neuritis is typically unilateral and transient but hypersensitivity, dominated by lymphocytes and may later recur in the same or the other eye. A high microglia. Various immunological effector mechanisms F proportion of affected individuals subsequently are initiated cytotoxic T-cell proliferation, antibody experience recurrent episodes of demyelination affecting production, and activation of microglia. These then act as different parts of the central nervous system. The risk is antigen-presenting cells, increasing the expression of further increased for those with cranial MRI class II major histocompatibility antigens and amplifying abnormalities at presentation.9 Serial clinical, the local inflammatory response. They engage opsonized electrophysiological, and imaging observations suggest myelin and oligodendrocytes, causing demyelination by a sequence in which inflammation leads to loss of vision cell–cell adherence and local release of inflammatory in association with impaired saltatory conduction mediators. As a result, the myelin–oligodendroctye unit through the normally myelinated optic nerve. As is damaged, saltatory conduction breaks down, and the inflammation subsides, conduction is restored and symptoms of multiple sclerosis follow. But this is not the vision improves.10 But structural damage may persist whole story. The impact of axonal injury has recently despite functional recovery. There is a reduction in been revisited and more fully defined. calibre of the optic nerve following a transient episode Clinical observations and related laboratory and of optic neuritis, indicating a loss of axonal density.11 experimental studies show that cytokines released by Yet vision improves rapidly and serial studies provide immune cells acting locally or in the systemic circulation some evidence for systematic reduction in latency of the induce transient conduction blockFin the optic nerve evoked potential consistent with remyelination of and elsewhere. In the unusual setting of monoclonal surviving axons.12 antibody therapy targeting the CD52 antigen, Thus, the study of optic neuritis has the potential lymphocytotoxicity leads to an acute cytokine release to illuminate the basic principles of symptom onset syndrome. This is associated with transient recurrence of and recovery, the dynamics of myelin and axonal many previously experienced symptoms and signs of injury, and the switch from clinically isolated to multiple sclerosis. Since the onset is abrupt and severe distributed demyelinating disease. The evidence but subsequent recovery is complete, it seems likely that suggests that (at least) three separate mechanisms of cytokines cause acute electrical failure in pathways symptom onset and three related but somewhat previously compromised by inflammation and different explanations for recovery interact to account demyelination. This interpretation is borne out by the for the complex pathogenesis of optic nerve and brain demonstration of transient blindness and loss of inflammation. conduction through the optic nerve in one patient who Eye Axon-glial injury of the optic nerve A Compston 1184 had recovered from a previous episode
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