JNNP: Expand the epitype of MOGAD-related diseases: half a century of epilepsy and relapsed optic neuritis

Autoimmune diseases open up a new field for the discovery of new esologics in clinical neurology.
the study of autoimmune pathophysiology led to successful treatment strategies, including long-term immunosuppression.
diseases associated with myelin-less protrusion glial cell glycoglobulin antibodies (MOGAD), damage to the central nervous system is associated with attack.
esoteric and extensibility of MOGAD."
here, the authors describe a new phenomenon in which the authors have followed the synchrotronity of steroid-reactive epilepsy and optic neuritis (ON) recurrence for 48 years in a Mogad sero-positive patient.
long-term follow-up of repeated imaging, electrodiagnosis and laboratory tests of blood and cerebrospinal fluids can be ruled out because of the association between common acute encephalitis attacks and ON.
the 69-year-old woman had repeated seizures, usually accompanied by a series of seizures before the attack.
48 years ago, she was diagnosed with epilepsy.
she currently suffers from severe nocturnal seizures, partially complex left frontal octresses, occasional tongue bites and/or brief convulsions in her limbs.
the next day, she was tired, but had never suffered from encephalopathy.
she also suffered periodic physical movements during her sleep, which left her paralysed from sleep.
repeated electro-encephalograms and polyseteric sleep maps always show possible left palpitations in the source area of epilepsy.
CT and MR brain imaging are normal.
nearly 20 years, she has had seizures three to four times a month.
after starting treatment with corticosteroids, the frequency of seizures was reduced to 3-5 per year.
sequence MRI scan showed that the left optic nerve had isolated reinforcement at the onset of the attack.
brain imaging was normal and there was no evidence of spinal cord disease.
ON has corticosteroid reactive and dependent, leading to clinical diagnosis as chronic relapse-inflammatory optic neuropathy (CRION).
her maintenance medications include psython and mycophenolate.
evidence of presumed autoimmune pathology for clinical diagnosis of CRION will not be proven until the correlation of MOG antibodies is rediscoered.
she tested positive for MOG sero twice.
, the newly reported relationship between MOGAD and acute encephalitis epilepsy was considered and ruled out.
Population analysis of water channel protein-4, N-methyl-D-tiantinine and voltage gated potassium channels, as well as anti-nuclear antibodies (ANA), anti-neutral granulocyte plasma antibodies (ANCA), and sub-tumor antibodies returned to normal.
clinically, doctors have recommended for the past 29 years to increase the dose of corticosteroids immediately when symptoms are detected to protect vision.
it is important to note that this usually prevents seizures.
, she began to document her seizures and seizures in detail (2015-2018).
the four-year observation period, it was clear that three-fifths of ON had seizures 1-2 days before the onset.
importantly, an increase in the dose of corticosteroids (10-20 mg once a day) always prevents seizures, and on three occasions, epilepsy relapses after oral corticosteroid reductions.
patient's two-sided disc pale.
-lying fault scans of macular macula showed severe atrophy of nerve cells and inner clumps, which have remained stable for the past six years.
kernel layer did not thicken, and there was no evidence of retrograde macular lesions (microcystic macular edema).
the seizure rate of MOGAD was 5%-21%, while the incidence of AQP4 antibody-positive optic neurospinalitis spectrum disorder (NMOSD) was 0.4%-1%.
three epilepsy manifestations of MOGAD are diverse, although most of them are ectopic seizures, but they are single-phase seizures, and MRI manifests itself as isolated or spreading encephalitis.
cases of MOGAD and epilepsy have been reported, but both are single-phase or bi-phase pathogenesis, with MRI manifesting it as inflammatory lesions.
3 patients initially performed normally, but soon developed a wider range of clinical and imaging disorders.
identification of serum proteins requires the investigation of MOG antibodies and the timely ongoing treatment of corticosteroids.
possible critical interval for starting corticosteroid use is within 48 hours of the on-the-look symptoms.
then slowly oral corticosteroids to test corticosteroid dependence.
the synchrons that affect outbreaks in different parts of the central nervous system are interdependent, and both diseases respond to immunosuppression.
Kleerekooper I, Trip SA, Plant GT, et al Expanding the phenotype of MOG antibody-associated disease (MOGAD): half a century of epilepsy and relapsing optic neuritis Journal of Neurology, Neurosurgery and Psimology Published Online First: 04 November 2020. doi: 10.1136/jnnp-2020-324323MedSci Original Source: MedSci Original Copyright Statement: All notes on this website "Source: Met Medical" or "Source: MedSci Original" text, pictures and audio and video materials, Copyright is owned by Mace Medical and may not be reproduced by any media, website or individual without authorization, with the following "Source: Met Medical" stated at the time of reprint.
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