Electrophysiological evidence for heterogeneity of lesions in optic neuritis.

PURPOSE To examine the natural history of multifocal visual evoked potentials (mfVEPs) within 12 months of the first episode of optic neuritis (ON) in patients with possible multiple sclerosis (MS). METHODS Twenty-seven patients with a first episode of ON, no previous demyelinating events, and MRI lesions consistent with demyelination were examined with mfVEP. Changes in amplitude and latency of mfVEP were analyzed at 1, 3, 6, and 12 months after an acute attack. RESULTS Five of 27 patients had persistent loss of amplitude after 12 months of follow-up. This loss was most marked centrally. Amplitude recovered in the remaining 22 patients at 1 month, but delayed latency, which was also most marked centrally, persisted. Of these, two distinct subgroups were identified: six patients with no improvement in latency and 16 patients with significant latency recovery over the 12 months of follow-up, suggesting remyelination. Conversion to MS was highest in the group with severe amplitude loss, followed by the group with no latency recovery. The conversion rate was lowest in the group of patients with latency improvement. CONCLUSIONS Distinct patterns of disease evolution were identified using mfVEP in patients with first episode of optic neuritis and at high risk for MS, supporting the concept of heterogeneity of early lesions in MS.

[1]  S. Klein,et al.  The topography of visual evoked response properties across the visual field. , 1994, Electroencephalography and clinical neurophysiology.

[2]  L. Kurland,et al.  Optic neuritis , 1995, Neurology.

[3]  S. Ludwin,et al.  Evidence for a “dying‐back” gliopathy in demyelinating disease , 1981, Annals of neurology.

[4]  M. Rodriguez Virus-induced demyelination in mice: "dying back" of oligodendrocytes. , 1985, Mayo Clinic proceedings.

[5]  P. Shrager,et al.  8 – Na+ Channel Reorganization in Demyelinated Axons , 2005 .

[6]  C. Dijkstra,et al.  Induction of nitric oxide synthase in multiple sclerosis lesions , 1997 .

[7]  R. Hidajat,et al.  Normalisation of visual evoked potentials after optic neuritis , 2003, Documenta Ophthalmologica.

[8]  R. Rudick,et al.  Axonal transection in the lesions of multiple sclerosis. , 1998, The New England journal of medicine.

[9]  H. Lassmann,et al.  Multiple sclerosis and chronic autoimmune encephalomyelitis: a comparative quantitative study of axonal injury in active, inactive, and remyelinated lesions. , 2000, The American journal of pathology.

[10]  S L Graham,et al.  Objective VEP Perimetry in Glaucoma: Asymmetry Analysis to Identify Early Deficits , 2000, Journal of glaucoma.

[11]  J. Parisi,et al.  Heterogeneity of multiple sclerosis lesions: Implications for the pathogenesis of demyelination , 2000, Annals of neurology.

[12]  S. Waxman,et al.  The Conduction Properties of Demyelinated and Remyelinated Axons , 2005 .

[13]  T A Sears,et al.  The internodal axon membrane: electrical excitability and continuous conduction in segmental demyelination. , 1978, The Journal of physiology.

[14]  B E Kendall,et al.  The pathophysiology of acute optic neuritis. An association of gadolinium leakage with clinical and electrophysiological deficits. , 1991, Brain : a journal of neurology.

[15]  Nitin Ohri,et al.  Detecting early to mild glaucomatous damage: a comparison of the multifocal VEP and automated perimetry. , 2004, Investigative ophthalmology & visual science.

[16]  Ivan Goldberg,et al.  Clinical application of objective perimetry using multifocal visual evoked potentials in glaucoma practice. , 2005, Archives of ophthalmology.

[17]  J. Frederiksen,et al.  Serial visual evoked potentials in 90 untreated patients with acute optic neuritis. , 1999, Survey of ophthalmology.

[18]  S. Graham,et al.  Multifocal topographic visual evoked potential: improving objective detection of local visual field defects. , 1998, Investigative ophthalmology & visual science.

[19]  R. Foster,et al.  Reorganization of the axon membrane in demyelinated peripheral nerve fibers: morphological evidence. , 1980, Science.

[20]  W. Mcdonald,et al.  The restoration of conduction by central remyelination. , 1981, Brain : a journal of neurology.

[21]  W. I. McDonald,et al.  Spontaneous and evoked electrical discharges from a central demyelinating lesion , 1982, Journal of the Neurological Sciences.

[22]  D. Chari,et al.  Remyelination In Multiple Sclerosis , 2007, International Review of Neurobiology.

[23]  Alastair Compston,et al.  McAlpine's Multiple Sclerosis , 2005 .

[24]  S L Graham,et al.  The diagnostic significance of the multifocal pattern visual evoked potential in glaucoma. , 1999, Current opinion in ophthalmology.

[25]  P M Matthews,et al.  Size-selective neuronal changes in the anterior optic pathways suggest a differential susceptibility to injury in multiple sclerosis. , 2001, Brain : a journal of neurology.

[26]  K. Frei,et al.  Mice with an inactivation of the inducible nitric oxide synthase gene are susceptible to experimental autoimmune encephalomyelitis , 1998, European journal of immunology.

[27]  V. Torri,et al.  Long-term follow-up of isolated optic neuritis: the risk of developing multiple sclerosis, its outcome, and the prognostic role of paraclinical tests , 1999, Journal of Neurology.

[28]  C. Raine,et al.  Multiple Sclerosis: Remyelination in Acute Lesions , 1993, Journal of neuropathology and experimental neurology.

[29]  B. Scheithauer,et al.  A quantitative analysis of oligodendrocytes in multiple sclerosis lesions. A study of 113 cases. , 1999, Brain : a journal of neurology.

[30]  S. Graham,et al.  Objective perimetry in glaucoma. , 2000, Ophthalmology.

[31]  Alexander Klistorner,et al.  Multifocal visual evoked potential latency analysis: predicting progression to multiple sclerosis. , 2006, Archives of neurology.

[32]  Rasa Ruseckaite,et al.  Sparse multifocal stimuli for the detection of multiple sclerosis , 2005, Annals of neurology.

[33]  M. Barnett,et al.  Relapsing and remitting multiple sclerosis: Pathology of the newly forming lesion , 2004, Annals of neurology.

[34]  A. Compston,et al.  Recommended diagnostic criteria for multiple sclerosis: Guidelines from the international panel on the diagnosis of multiple sclerosis , 2001, Annals of neurology.

[35]  S. Graham,et al.  Multifocal objective perimetry in the detection of glaucomatous field loss. , 2002, American journal of ophthalmology.

[36]  G. Ebers,et al.  Optic Neuritis and Multiple Sclerosis , 1983, Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques.

[37]  A. Thompson,et al.  The prognostic value of brain MRI in clinically isolated syndromes of the CNS. A 10-year follow-up. , 1998, Brain : a journal of neurology.

[38]  W. Mcdonald,et al.  The pathophysiology of multiple sclerosis , 2006 .

[39]  Michael Wall,et al.  High- and low-risk profiles for the development of multiple sclerosis within 10 years after optic neuritis: experience of the optic neuritis treatment trial. , 2003, Archives of ophthalmology.

[40]  Chris A. Johnson,et al.  Determining abnormal latencies of multifocal visual evoked potentials: a monocular analysis , 2004, Documenta Ophthalmologica.

[41]  D. Hood,et al.  Tracking the recovery of local optic nerve function after optic neuritis: a multifocal VEP study. , 2000, Investigative ophthalmology & visual science.

[42]  W. Mcdonald,et al.  Delayed visual evoked response in optic neuritis. , 1972, Lancet.

[43]  Moses Rodriguez Virus-induced demyelination in mice , 1985 .

[44]  Stephen J. Jones,et al.  Long-term remyelination after optic neuritis: A 2-year visual evoked potential and psychophysical serial study. , 2001, Brain : a journal of neurology.

[45]  Gordon T. Plant,et al.  Long-term recovery and fellow eye deterioration after optic neuritis, determined by serial visual evoked potentials , 1999, Journal of Neurology.

[46]  C. Lucchinetti,et al.  Remyelination in multiple sclerosis , 1997, Multiple sclerosis.

[47]  S. Graham,et al.  Multifocal visual evoked potential analysis of inflammatory or demyelinating optic neuritis. , 2006, Ophthalmology.

[48]  S G Waxman,et al.  Multiple sclerosis as a neuronal disease. , 2005, Archives of neurology.

[49]  D. Hood,et al.  Improvement in conduction velocity after optic neuritis measured with the multifocal VEP. , 2007, Investigative ophthalmology & visual science.

[50]  J. Parisi,et al.  The pathology of multiple sclerosis: evidence for heterogeneity. , 2006, Advances in neurology.

[51]  S L Graham,et al.  Electroencephalogram-based scaling of multifocal visual evoked potentials: effect on intersubject amplitude variability. , 2001, Investigative ophthalmology & visual science.

[52]  T A Sears,et al.  The effects of experimental demyelination on conduction in the central nervous system. , 1970, Brain : a journal of neurology.

[53]  V. Perry,et al.  Axonal damage in acute multiple sclerosis lesions. , 1997, Brain : a journal of neurology.

[54]  H. Lassmann,et al.  Autoimmunity to Myelin Oligodendrocyte Glycoprotein in Rats Mimics the Spectrum of Multiple Sclerosis Pathology , 1998, Brain pathology.

[55]  Steve J Jones,et al.  Neurophysiological evidence for long-term repair of MS lesions: implications for axon protection , 2003, Journal of the Neurological Sciences.

[56]  Michael Wall,et al.  MRI predictors of early conversion to clinically definite MS in the CHAMPS placebo group , 2002, Neurology.