Functional MRI as a tool for assessing chiasmal visual defect in a patient with neuromyelitis optica

Raz, Noa; Vaknin, Adi; Chokron, Sylvie; Ben‐Hur, Tamir; Levin, Netta

doi:10.1136/jnnp.2009.183749

Cited by 13 publications

(11 citation statements)

References 4 publications

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“…In NMOSD, ON often spans several segments of the optic nerve, and chiasmal crossover is reported in some cases 37. In our study, 3.3% of eyes without history of ON showed severely reduced GCIP at baseline, indicative of chiasmal affection and crossing-over during acute ON, which was clinically apparent only unilaterally.…”

Section: Discussionsupporting

confidence: 43%

Retinal ganglion cell loss in neuromyelitis optica: a longitudinal study

Oertel

Havla

Roca-Fernández

et al. 2018

J Neurol Neurosurg Psychiatry

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This study clearly shows GCIP loss independent of ON attacks in aquaporin4-antibody-seropositive NMOSD. Potential explanations for progressive GCIP thinning include primary retinopathy, drug-induced neurodegeneration and retrograde neuroaxonal degeneration from lesions or optic neuropathy. pRNFL thickening in the patients presenting with attacks during F/U might be indicative of pRNFL susceptibility to inflammation.

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Section: Discussionsupporting

confidence: 43%

Retinal ganglion cell loss in neuromyelitis optica: a longitudinal study

Oertel

Havla

Roca-Fernández

et al. 2018

J Neurol Neurosurg Psychiatry

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“…While magnetic resonance imaging (MRI) shows changes typical of acute ON, such as optic nerve enlargement, T2 hyperintensity, and gadolinium enhancement, the lesions are often more extensive and likely to involve the optic chiasm or adjacent hypothalamus (Figure 2A; Li et al, 2008). NMO ON generally causes more severe visual field defects than MS ON (Fernandes et al, 2012a), and, given its potential to involve the optic chiasm and tracts, may manifest with bitemporal or homonymous visual field defects (Raz et al, 2010; Costa et al, 2007; Romero et al, 2012). With the more routine serologic testing of individuals with acute optic neuritis, the spectrum of visual symptoms associated with NMO ON may expand over time.…”

Section: Clinical Features Of Nmomentioning

confidence: 99%

Optic neuritis in neuromyelitis optica

Levin

Bennett

Verkman

2013

Progress in Retinal and Eye Research

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Neuromyelitis optica (NMO) is an autoimmune demyelinating disease associated with recurrent episodes of optic neuritis and transverse myelitis, often resulting in permanent blindness and/or paralysis. The discovery of autoantibodies (AQP4-IgG) that target aquaporin-4 (AQP4) has accelerated our understanding of the cellular mechanisms driving NMO pathogenesis. AQP4 is a bidirectional water channel expressed on the plasma membranes of astrocytes, retinal Müller cells, skeletal muscle, and some epithelial cells in kidney, lung and the gastrointestinal tract. AQP4 tetramers form regular supramolecular assemblies at the cell plasma membrane called orthogonal arrays of particles. The pathological features of NMO include perivascular deposition of immunoglobulin and activated complement, loss of astrocytic AQP4, inflammatory infiltration with granulocyte and macrophage accumulation, and demyelination with axon loss. Current evidence supports a causative role of AQP4-IgG in NMO, in which binding of AQP4-IgG to AQP4 orthogonal arrays on astrocytes initiates complement-dependent and antibody-dependent cell-mediated cytotoxicity and inflammation. Immunosuppression and plasma exchange are the mainstays of therapy for NMO optic neuritis. Novel therapeutics targeting specific steps in NMO pathogenesis are entering the development pipeline, including blockers of AQP4-IgG binding to AQP4 and inhibitors of granulocyte function. However, much work remains in understanding the unique susceptibility of the optic nerves in NMO, in developing animal models of NMO optic neuritis, and in improving therapies to preserve vision.

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“…The evaluation of the optic nerve in NMO/NMOSD patients with acute ON should be performed with specific orbital studies using acquisitions such as short tau inversion recovery, T2 and T1 with gadolinium to evaluate the lesion extension and the presence of contrast-enhancing lesions. Chiasmal and optic tract MRI lesions have also been reported in NMO/NMOSD (24,109,110). These long, edematous lesions are usually associated with severe visual loss and may be found in bilateral ON.…”

Section: Mri Neuro-ophthalmological and Laboratory Findings In Nmo/nmentioning

confidence: 96%

“…In the sole published study using Goldmann perimetry, the authors found a central scotoma in 54% of the NMO/NMOSD and 90% of the MS patients (93). VF examination may also disclose bitemporal and homonymous hemianopsias suggesting chiasmal and retrochiasmal involvement in NMO/NMOSD (24,109,110). Automated perimetry, on the other hand, showed a more severe diffuse loss of visual sensitivity in NMO/NMOSD than in MS. Sectorial defects were not different in MS and NMOSD (30).…”

Section: Visual Field (Vf)mentioning

confidence: 98%

Clinical Spectrum and Treatment of Neuromyelitis Optica Spectrum Disorders: Evolution and Current Status

et al. 2013

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Neuromyelitis optica (NMO) is an inflammatory neurologic disease clinically characterized by severe optic neuritis (ON) and transverse myelitis (TM). The relationship between NMO and multiple sclerosis (MS) has long been a matter of debate. However, the discovery of an NMO-specific autoantibody, NMO-immunoglobulin G/aquaporin 4 (AQP4) antibody, has dramatically advanced our understanding of the disease, and the clinical, magnetic resonance imaging (MRI), optical coherence tomography, and laboratory examinations have clarified unique features of NMO that are distinct from MS. The term NMO spectrum disorders (NMOSD) incorporating spatially limited forms was introduced, as patients with recurrent or simultaneous bilateral ON or recurrent longitudinally extensive TM (LETM) alone are also often AQP4 antibody-seropositive. Moreover, studies of seropositive cases have shown that more than half of them have brain lesions, some of which are unique to NMO, and can be the onset manifestation. Some clinical features of AQP4 antibody-seronegative NMO differ from seropositive, but it remains unknown whether they are pathologically distinct. Immunosuppressive treatments are effective for acute attacks and prevention of relapses of NMOSD, and new molecularly targeted drugs are under investigation. Importantly, some disease modifying drugs for MS may exacerbate NMOSD, making early differential diagnosis of the two diseases crucial. We review the evolving clinical spectrum, the updated clinical, MRI, neuro-ophthalmological and laboratory findings, and the current status of treatment in NMOSD.

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Functional MRI as a tool for assessing chiasmal visual defect in a patient with neuromyelitis optica

Cited by 13 publications

References 4 publications

Retinal ganglion cell loss in neuromyelitis optica: a longitudinal study

Retinal ganglion cell loss in neuromyelitis optica: a longitudinal study

Optic neuritis in neuromyelitis optica

Clinical Spectrum and Treatment of Neuromyelitis Optica Spectrum Disorders: Evolution and Current Status

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