Axonal electrovisiogram or inverse photopic skin electroretinogram?

Messias, Katharina; Castro, Vivian Carla de; Gekeler, Florian; Messias, André

doi:10.1590/s0004-27492012000500017

Cited by 3 publications

(13 citation statements)

References 2 publications

(4 reference statements)

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“…Patients often complained of signi cant eye pain. In the acute stage, there was a sharp decrease in vision and visual eld defect in one or both eyes (5) The results of this study showed that although high antibody titers at the beginning of the disease may also have the possibility of faster recovery, the treatment time of MOGAD patients with different titers was inconsistent (p 0.001, the difference was statistically signi cant). Therefore, this result suggested that the level of antibody was related to the treatment time.…”

Section: Discussionmentioning

confidence: 69%

Differences in clinical features, disease outcomes and imaging features of demyelinating syndrome after MOG antibody therapy

Li¹,

Shang²

2023

Preprint

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Objective: To strengthen the clinicians' understanding of the clinical characteristics of patients with negative MOGADD antibody. Methods: The clinical data of 23 MOGADD patients with antibody negative conversion who were hospitalized in the Department of Neurology, the First Affiliated Hospital of China Medical University in Shenyang, Liaoning Province from March 2020 to August 2022 were retrospectively analyzed. The general situation, clinical characteristics, laboratory tests, imaging data, antibodies, treatment and follow-up of the patients were analyzed and summarized. Results: The clinical data of 23 patients with MOGADD were retrospectively analyzed. Most of the patients were adult women, and the onset was vision loss. For the 9 MOGAD patients who turned negative after MOGAD treatment (98.9±26.2 days), the treatment time for the antibody turned negative in the earliest one month and the most recent four months was much shorter than that for the 14 persistent MOGAD positive patients (146.7±27.8 days) (p＜ 0.001, statistically significant difference) suggested that the MOGAD therapy-negative group recovered faster than the MOGAD persistently positive group. The treatment time of MOGADD patients with different titers was inconsistent (p＜0.001, the difference was statistically significant) suggested that the higher the titer in the MOGAD treatment negative group, the later the antibody turned negative, and the higher the titer in the persistent MOGAD positive group, the longer the treatment duration. MOGADD patients had increased cerebrospinal fluid chloride (p＜0.05, the difference was statistically significant)suggested that compared with the MOGAD persistent positive group, the increase of cerebrospinal fluid protein was more common in the MOGAD who turned negative after MOGAD treatment, and the MOGAD persistent positive group had more increased cerebrospinal fluid chloride. In the MOGAD treatment negative group, there were multiple long T2 signal shadows in the head (6/9 cases) and multiple short-segment lesions in the spinal cord MRI, while in the MOGAD continuous positive group, there were multiple patchy long T2 signal shadows and more common in the pons (3/14 cases), and most of the spinal cord MRI of the patients were diffuse long segment and single lesion (p＜0.05, the difference was statistically significant). Therefore, it is concluded that, different from the long segment and single lesion in the spinal cord MRI of the MOGAD continuous positive group, the head MRI lesions of the MOGAD treatment negative group are mostly in the pons and the spinal cord lesions are mostly short segment and multiple lesions. Among the 23 MOGAD patients in this study, 14 (14/23 cases) recurs after MOGAD treatment. The number of MOGAD negative group (1/9 cases) was much less than that of MOGAD persistent positive group (13/14 cases) (p＜0.001, the difference was statistically significant), which suggested that the recurrence rate in the MOGAD who turned negative after MOGAD treatment (11.1%) was much lower than that in the MOGAD who remained positive (92.9%). Conclusion: Compared with antibody-positive patients, antibody-negative MOGADD patients have their own clinical and imaging characteristics, low recurrence rate and good prognosis.

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Section: Discussionmentioning

confidence: 69%

Differences in clinical features, disease outcomes and imaging features of demyelinating syndrome after MOG antibody therapy

Li¹,

Shang²

2023

Preprint

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“…Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a recently defined inflammatory demyelinating disease, that generally affects the optic nerve (ON) in adults and the central nervous system in children 1 , 2 . The specific clinical phenotype, radiological findings, and neurological manifestations enable its distinction from other central nervous system inflammatory demyelinating diseases (CNS IDDs) such as aquaporine-4-IgGQ neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS) 3 4 5 .…”

Section: Introductionmentioning

confidence: 99%

“…Other neurological symptoms found in MOGAD include pain on ocular movements, brainstem symptoms with headache, nausea, or vomiting, as well as myelitis or cortical lesions with seizures or cranial nerve involvement 1 .…”

mentioning

confidence: 99%

A Difficult Case of Optic Neuropathy: Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD)

Haeller,

Badoux,

Medlin

et al. 2024

Klin Monbl Augenheilkd

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“…Axons comprising the ON extend from retinal ganglion cells (RGCs), and demyelination of these axons induces RGC apoptosis. ADON is commonly monocular and lesion localization is retrobulbar in MS [26] . Although most pwMS recover vision following the resolution of inflammation, recurrent flare-ups can culminate in irreversible vision loss.…”

Section: Introductionmentioning

confidence: 99%

“…First-line treatment for acute attacks is intravenous steroids, which accelerate recovery for some patients but fail to impact relapse frequency [27] . Second-line treatments include plasma exchange, IV immune globulin, and other agents (reviewed in [17,26,[28][29][30] ). Proper diagnosis is paramount as several highly-prescribed MS treatments (eg, glatiramer acetate, interferon β (IFN-β), fingolimod, and dimethyl fumarate) can worsen conditions for people with NMO or MOG-ADs [17,31,32] .…”

Section: Introductionmentioning

confidence: 99%

Overview of diet and autoimmune demyelinating optic neuritis: a narrative review

Plafker¹,

Titcomb²,

Zyla-Jackson³

et al. 2023

Immunometabolism

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This review summarizes the cellular and molecular underpinnings of autoimmune demyelinating optic neuritis (ADON), a common sequela of multiple sclerosis and other demyelinating diseases. We further present nutritional interventions tested for people with multiple sclerosis focusing on strategies that have shown efficacy or associations with disease course and clinical outcomes. We then close by discuss the potential dietary guidance for preventing and/or ameliorating ADON.

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Axonal electrovisiogram or inverse photopic skin electroretinogram?

Cited by 3 publications

References 2 publications

Differences in clinical features, disease outcomes and imaging features of demyelinating syndrome after MOG antibody therapy

Differences in clinical features, disease outcomes and imaging features of demyelinating syndrome after MOG antibody therapy

A Difficult Case of Optic Neuropathy: Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD)

Overview of diet and autoimmune demyelinating optic neuritis: a narrative review

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