3.2 Laboratory characteristics
Lumbar puncture was performed in all patients. Elevated intracranial
pressure (>180 mm H20) was observed in 7/10
patients with a median of 176.8 mm H20 (range: 90–280).
CSF analysis showed pleocytosis (>8 white cell count/μl) in
9/10 patients with a median white blood cell (WBC) count of 63.9
cells/μl (range: 0–320), and monocytes dominated WBC. CSF protein was
elevated in 4/10 patients with a median of 426.1 mg/L (range:
162–1311). Five patients were tested for oligoclonal bands (OCBs), and
three (60%) showed positive results, with increasing bands restricted
to the CSF (Pattern II).
During the first clinical attack, serum MOG antibody was detected in 5
patients (one was weakly positive in CSF), and anti-NMDAR antibody was
detected in the CSF of 9 patients and serum of 4 patients (Table 1). In
our study, all 10 patients experienced relapses with new or recurrent
symptoms. Thus, we defined a relapse phase based on the following
conditions: 1) a clinical attack with symptoms different from previous
presentations or similar symptoms recurring; 2) the clinical progression
(worsening neurological deficit) was paralleled with serum/CSF
autoantibody positivity; and 3) the new episode occurred more than 30
days following the onset of previous attack.
When relapse occurred, the patients with encephalitis or demyelination
were tested for both MOG and anti-NMDAR antibodies. We found that five
patients showed previous anti-NMDAR-IgG positivity followed by
anti-MOG-IgG positivity, four patients presented with dual anti-NMDAR
and anti-MOG positivity simultaneously, and only one patient presented
MOG serum positivity and secondary NMDAR encephalitis. Interestingly,
when analyzing clinical relapses with antibody dynamics, we found that
MOG-IgG played a dominant pathogenic role in relapse episode with higher
antibody titers compared with anti-NMDA-IgG (p < 0.01) (Figure
2A), which indicated altering of MOG titers showed more relevant to
clinical relapse. In the relapse episodes, the major symptoms included
decreased vision (3/10), double vision (3/10), mental symptoms (3/10)
(proportion described in Figure 2B).