Clinical analysis of a patient simultaneously positive for antibodies of myelin oligodendrocyte glycoprotein and anti-N-methyl-D-aspartate receptor: A case report

Abstract

Rationale: Myelin oligodendrocyte glycoprotein (MOG) antibody (MOG-Ab) disease (MOG-AD) is a type of demyelinating disease of the central nervous system characterized by a high frequency of optic neuritis (ON) attacks. anti-Nmethyl-D-aspartate receptor (NMDAR) encephalitis (anti-NMDARe) is an autoimmune disorder characterized by memory deficits, conscious disturbance, and seizures. Cases of simultaneous occurrence of MOG-Ab and anti-NMDARe antibody (anti-NMDARe-Ab) are rarely reported and could be mistaken for overlapping MOG-antibody disease (MOG-AD) and NMDARe. The diagnosis of such patients is challenging.

Patient concerns: We report the case of a 37-year-old man who presented with recurrent headaches for 3 months and worsening symptoms over 2 weeks. He had a history of ON. He had a generalized seizure after 7 days in the hospital.

Diagnosis: Brain magnetic resonance imaging (MRI) and cerebrospinal fluid tests showed no apparent abnormalities. Repeat MRI showed slight lesions 7 days later, and cerebrospinal fluid tests showed the simultaneous occurrence of MOG-Ab and anti-NMDARe-Ab.

Interventions: He completely recovered after treatment with low doses of oral corticosteroids.

Outcomes: Two months and 2 years follow-up showed that his condition was stable.

Lessons: The co-occurrence of MOG-Ab and anti-NMDAR-Ab does not indicate the co-occurrence of MOG-AD and anti-NMDARe. Laboratory findings should be combined with the clinical features to achieve an accurate and suitable diagnosis.

Figure 1

Magnetic resonance (MR) images of the brain and cervical spine. An initial fluid-attenuated inversion recovery (FLAIR) image (A), brain MR angiography (B), brain MR venography (C), and cervical spine MR images (D). All show no obvious abnormalities. Repeated FLAIR image after the condition worsened, demonstrating an abnormal hyperintense signal in the medial aspect of the bilateral frontal lobes and involvement of the cingulate cortex (E and F, arrows); a gadolinium-enhanced T1-weighted image showing enhancement in the parts above the lesions (G, arrow); and abnormal enhanced meninges (H, arrow).

Figure 2

(Graphical abstract) Timeline of the patient's disease course. Abs = antibodies, Anti-NMDAR = anti-N-methyl-D-aspartate receptor, CSF = cerebrospinal fluid, MRI = magnetic resonance imaging, ON = optic neuritis, WBC = white blood cells.

Figure 3

The hypothesized mechanism of action of an autoimmune reaction to MOG-AD. The MOG-antigen leaks into the peripheral blood when the blood–brain barrier is destroyed by a neurotropic viral infection. T helper cells are activated, which increases the recruitment and activation of specific B cells for MOG, which, in turn, produces a large number of MOG-Ab, causing injury to MOG in the myelin sheath and, ultimately, leading to MOG-AD. AD = antibody disease, MOG = myelin oligodendrocyte glycoprotein. Note: This figure is our own.