Table 3.
References | Number of cases | Sex/age |
|
Overlapping autoimmunity and/or autoantibodies | Notable clinical features, or MRI findings | |
---|---|---|---|---|---|---|
Mader et al. (2011)67 | 2 | NA/NA |
|
SLE | ||
Mader et al. (2018)89 | 3 | NA/NA |
|
Demyelinating or non-demyelinating NPSLE | All patients with demyelinating NPSLE met the ACR 1999 criteria for demyelination, and all had either TM occurring at 2 different time points or TM with WM demyelination or ON occurring at two different time points. | |
Bilodeau et al. (2019)90 | 1 | F/32 |
|
SLE | Presented with severe TM (paraplegia) shortly after SLE onset in the post-partum period. FLAIR MRI showed lesions in medulla, pons, hypothalamus, subcortical WM, and T2-hyperintense lesions adjacent to the third and fourth ventricle. Spinal MRI showed LETM in the entire cervical and thoracic cord. | |
Pröbstel et al. (2019)91 | 14 | M/34 F/33 F/61 F/35 F/63 F/49 F/51 F/34 M/54 F/26 F/35 F/31 F/25 M/40 |
|
NPSLE (N = 6) and
non-NPSLE (N = 8) |
Presentation of visual disturbance, bladder dysfunction, seizure, and psychosis. | |
ANA Anti-ds-DNA Anti-Phospholipid Anti-Sm Anti SSA/SSB |
N = 14N = 9N = 8N = 3N = 2 | |||||
Seth et al. (2020)92 | 11 | NA/NA |
|
NPSLE (N = 8) and
non-NPSLE (N = 3) |
MOG-IgG was positive in a significantly higher proportion of patients having mood disorder as compared to patients without it. | |
Chawla et al. (2021)93 | 1 | F/33 |
|
Development of MOG-LETM in a patient with SLE, during active COVID-19 | Presents with numbness and weakness in bilateral lower extremities with associated diplopia, urinary retention, 10 days after diagnosis of COVID-19 infection.T2-FLAIR brain MRI showed hyperintense lesions in the superior and middle cerebellar peduncles. MRI of spine showed LETM involving C4-C7 and T11-T12. | |
Kunchok et al. (2019)25 | 51 | NA/NA |
|
ANA Ds-DNA ENA Anti-CASPR2-IgG and LGI1-IgG antibodies GABA-A-R-IgG ATD RA Vitiligo Sjogren Pernicious anemia APS |
N = 17 N = 3 N = 7 N = 1 N = 1 N = 14 N = 1 N = 1 N = 1 N = 1 N = 1 |
|
Kunchok et al. (2021)3 | 38 (from total of 170 MOGAD patients) | NA/NA | MOGAD Either flow cytometric assay or CBA | ANA ds-DNA Anti-Sm RNP RA SLE ATD Sjogren |
N = 13 N = 5 N = 1 N = 3 N = 2 N = 1 N = 12 N = 1 |
|
Malli et al. (2021)94 | 17 | NA/NA |
|
ANA ATD/thyroid Autoantibody Atopic dermatitis |
N = 9 N = 5 N = 4 |
All autoantibodies: IIF, Presenting with NMOSD, recurrent TM, recurrent ON, and ADEM. |
Jarius et al. (2016)95 | 19 | NA/NA |
|
ANA ANCA ACA or B2GP RF anti-TPO anti-TG Anti-TSHR (perinuclear) tTg-IgA RA ATD Atopic dermatitis Asthma bronchiole |
N = 14 N = 1 N = 2 N = 1 N = 2 N = 1 N = 1 N = 1 N = 2 N = 2 N = 1 N = 1 |
|
Ramanathan et al. (2018)96 | 4 | NA/NA |
|
Type 1 DM and Hashimoto's thyroiditis Elevated thyroid Abs Henoch-Schönlein purpura Anti-LGI1 Abs |
N = 1 N = 1 N = 1 N = 1 |
|
Sato et al. (2014)7 | 5 | M/29 F/15 M/49 M/70 M/38 |
|
ANA Anti-SSA Anti-TG Anti-TPO |
N = 1 N = 1 N = 1 N = 1 |
|
Zhou et al. (2019)20 | 6 | NA/NA |
|
ANA Anti-TPO |
N = 5 N = 1 |
|
Veselaj et al. (2021) 97 | 7 | F/25 F/21 M/66 F/40 F/58 F/17 M/55 |
|
ANA Autoimmune hepatitis Undifferentiated connective tissue disease with positive ANA Chronic juvenile arthritis ANA and P-ANCA |
N = 3 N = 1 N = 1 N = 1 N = 1 |
|
Chen et al. (2021)56 | 8 | NA/NA |
|
Anti-TPO/TG ANA Anti-SSA Anti-SSB Anti-RO-52 |
N = 4 N = 1 N = 1 N = 1 N = 1 |
|
Song et al. (2019)98 | 23 | NA/NA |
|
ANA Anti-centromere Abs Anti-SSA/SSB Anti-CL/β 2GPI Anti-perinuclear factor Abs Anti-TG/TPO |
N = 6 N = 2 N = 3 N = 6 N = 2 N = 4 |
|
James et al. (2020)99 | 1 | F/39 |
|
ANA + anti-SSB Abs | ||
Stathopoulos et al. (2019)100 | 9 | NA/NA |
|
RA Type 1 DM SLE |
N = 5 N = 2 N = 2 |
|
Zhao et al. (2018)101 | 4 | NA/NA |
|
ANA Anti-SSA/SSB |
N = 3 N = 1 |
|
Ciotti et al. (2020)102 | 6 | NA/NA |
|
ANA ENA |
N = 5 N = 1 |
|
Papathanasiou et al. (2020)103 | 4 | NA/NA M/40 M/23 |
|
ANCA P-ANCA with PR3-ANCA GAD-Ab |
N = 3 N = 1 N = 1 |
|
Soelberg et al. (2018)104 | 1 | NA/NA |
|
Anti-Sm antibody (weakly positive) | ||
Cross et al. (2021)105 | 3 | M/39 F/33 M/40 |
|
ATD, psoriasis | ||
Liu et al. (2021)106 | 2 | NA/NA |
|
ATD Psoriasis |
N = 1 N = 1 |
|
Cobo-Calvo et al. (2016)107 | 1 | NA/NA |
|
MG | ||
Chen et al. (2017)108 | 1 | F/10 |
|
Hashimoto thyroiditis encephalitis | Preceding autoimmune thyroid disease with elevated circulating
anti-thyroid Abs, followed by subacute onset of multifocal CNS
dysfunction. Brain MRI showed asymmetric, multifocal regions of T2-W and FLAIR signal hyperintensity in the subcortical white matter, left globus pallidus, thalami, midbrain, left pons, and cerebellum. |
|
Nagahata et al. (2022)109 | 1 | F/63 |
|
|
Presentation of recurrent poor vision and hearing loss with MRI showing low contrast-enhanced right optic nerve sheath and contrast-enhanced cavernous sinusitis. | |
Vural et al. (2017)80 | 2 | NA/NA |
|
Sjogren's syndrome | ||
Jobling et al. (2019)110 | 1 | M/13 |
|
Sjogren's syndrome with positive anti-Ro and anti-La | Presentation of TM following a severe upper respiratory system infection. MRI showed a subtle TM of conus medullaris. | |
Ling et al. (2020)111 | 1 | F/53 |
|
Sjogren's syndrome and positive SSA, ANA, RF | Acute ON with MRI finding of mild right optic nerve enhancing lesion and normal brain MRI, 8 years after diagnosis of Sjogren which presented with BON. | |
Mittal et al. (2021)112 | 1 | F/32 |
|
Sjogren disease with positive ANA, anti-Ro, anti-RNP | Left optic neuritis with intraretinal and subretinal hemorrhages. MRI showed T2 hyperintensity and expansion of the left optic nerve and nerve sheath, along with flattening of the globe at the nerve insertion, and contrast enhancement of left optic nerve and sheath on T1. | |
Stamenova et al. (2021)113 | 1 | F/31 |
|
Crohn's disease treated with TNF-alpha inhibitors (adalimumab) and azathioprine | Development of headache, fever, and left-sided focal motor seizures, which progressed to bilateral tonic-clonic seizures during pregnancy. MRI showed bilateral cortical FLAIR-hyperintense lesions. | |
Philippart et al. (2019)114 | 1 | M/33 |
|
Crohn's disease treated with TNF-alpha inhibitors (adalimumab) and azathioprine | Recurrent myelitis and brainstem syndrome with non-enhancing T2 hyperintense lesion from T4 to T6, and a second T2 hyperintensity at the T2 level. Brain MRI unremarkable. | |
Luo et al. (2021)115 | 1 | F/26 |
|
Ankylosing spondylitis treated with TNF-alpha inhibitors (adalimumab) | Left ON and TM in postpartum setting, in a patient with AS treated with TNF-alpha inhibitors (adalimumab). T2-W MRI showed high signal intensity within the left optic nerve and the spinal cord from C5 to T2. No lesions were found in the brain. | |
Lommers et al. (2018)116 | 1 | M/40 |
|
Pustular psoriasis treated with TNF-alpha inhibitors | MRI showed LETM at the bulbo-medullar junction with gadolinium enhancement in first attack, and T2 hyperintense signal in the intra-orbital part of the left optic nerve with a discrete enhancement in second attack. | |
Takei et al. (2017)117 | 1 | F/18 |
|
Atopic dermatitis | Development of left-side dominant diffuse muscle weakness and numbness with bilateral ankle pseudo clonus along with deterioration of atopic dermatitis, followed by left ON one month later. MRI showed no abnormal lesions except for slight enlargement of the central canal at T7. | |
Adhikari et al. (2021)118 | 1 | F/26 |
|
Opsoclonus myoclonus syndrome | Progressive bilateral hand tremors, intermittent myoclonus, ataxia, vertigo, and opsoclonus for two weeks in postpartum setting, found to be MOG-IgG positive in the second relapse, four months later. MRI showed non-enhancing right periventricular and left globus pallidus T2 FLAIR hyperintensities in initial presentation, and two new bilateral subcortical hyperintensities, one with postcontrast enhancement in second relapse. | |
Baptista et al. (2017)119 | 20 | NA/NA |
|
RA | Patients had significantly higher levels of anti-MOG-IgG (5.68 ± 1.34 vs 0.51 ± 0.49 ng/mL), than controls. | |
Martinez-Hernandez et al. (2015)72 | 3 | M/27 F/27 M/11 |
|
|
||
Hacohen et al. (2016)120 | 1 | NA/NA |
|
|
||
Armangue et al. (2017)121 | 4 | NA/NA |
|
|
Children with acquired demyelinating syndrome with positive MOG-IgG had less frequent periventricular and tectum lesions, but more diffuse cerebellum involvement. | |
Ding et al. (2020)122 | 1 | M/20 |
|
|
||
Fang et al. (2021)123 | 4 | NA/NA |
|
|
||
Ji et al. (2021)124 | 1 | 23/F |
|
|
Presentation of transient convulsions, a loss of consciousness, persistent fever, and vomiting, misdiagnosed as infectious meningoencephalitis. MRI showed asymmetric lesions of cerebellum, corona radiata, and enhancing white matter lesions. | |
Zhao et al. (2020)125 | 1 | F/30 |
|
|
Normal brain and orbital imaging | |
Martin et al. (2022)126 | 1 | M/53 |
|
|
Presentation of isolated meningitis and papillitis. | |
Shimizu et al. (2019)127 | 10 | NA/NA |
|
|
The rate of GRP78 antibody positivity observed in acute MOG groups (10/15, 66%) was significantly higher than that in the disease control groups (3/27, 11%) or the healthy control groups (0/9, 0%). | |
Liu et al. (2020)128 | 1 | F/48 |
|
|
Decreased vision in the right eye and subsequent episodes of neuropsychiatric disturbance including hypersomnia, agitation, apatheia, and memory impairment, with T2 and FLAIR hyperintense multiple lesions scattered in brain, brainstem, and cervical and thoracic spinal cord, with heterogenous patchy or ring-like enhancement in the majority of lesions. | |
Rauer et al. (2006)129 | 15 | NA/NA |
|
|
There was no increased risk for developing definite MS in CIS patients with positive anti-MOG/MBP antibodies. | |
Tomassini et al. (2007)130 | 13 | F (N = 11), M
(N = 2) Median age: 27 years (range 25–33) |
|
|
Presentation of MOG-IgG-associated ON (N = 4), BS-cerebellar syndrome (N = 3), myelitis (N = 3), and multifocal neurologic deficit (N = 3). Patients with double seropositivity had a higher risk of second relapse compared to seronegative or single seropositive patients. | |
Rinaldi et al. (2021)131 | 4 | F/30 F/29 M/58 F/31 |
|
|
Coexistence of central and peripheral nervous system involvement in MOGAD patients. | |
Li et al. (2022)132 | 1 | M/33 |
|
|
Presentation of FLAIR hyperintense lesions in MOG-IgG-associated encephalitis and seizures (FLAMES). |
Abbreviations: SLE: systemic lupus erythematosus; NPSLE: neuro-psychiatric SLE; ANA: anti nuclear antibody; ds-DNA: double-strand DNA; Anti-Sm: Anti-smith; ENA: extractable nuclear antigen antibodies; GABA-A-R: gamma aminobutyric acid receptor; CASPR2: contactin-associated protein-like 2; LGI1: leucine-rich glioma-inactivated 1; ATD: autoimmune thyroid disease; RA: rheumatoid arthritis, APS: anti-phospholipid syndrome; RNP: ribonucleoprotein; ANCA: antineutrophil cytoplasmic antibodies; ACA: anticardiolipin; B2GP: beta(2) glycoprotein; RF: rheumatoid factor; TPO: thyroid peroxidase antibody; TG: thyroglobulin; TSHR: thyroid stimulating hormone receptor; tTg: tissue transglutaminase; Anti-CL: anti-cardiolipin; PR3: proteinase3; GAD: Glutamic acid decarboxylase-antibody; MG: Myasthenia gravis; MPO: Myeloperoxidase; AS: Ankylosing spondylitis; GlyRs-Ab: Glycine receptor antibody; GRP78: Glucose regulated protein 78; MBP: myelin basic protein; NF155: neurofascin155; GM1: ganglioside epitope.