No abstract

A 74-year-old woman who exhibited drowsiness was referred to our hospital. Enhanced head magnetic resonance imaging (MRI) revealed multiple ring-enhancing lesions and lesions showing partial mild hemorrhaging. The patient gradually progressed to a comatose condition with notable brain deterioration of unknown cause on follow-up MRI. On day nine, the patient inexplicably died, although brain herniation was suspected. Autopsy and histopathology revealed numerous amoebic trophozoites in the perivascular spaces and within the necrotic tissue. Brain immunostaining tested positive for Balamuthia mandrillaris. Infection due to free-living amoeba is rare in Japan; however, it may increase in the near future due to unknown reasons.

Background Anti-myelin oligodendrocyte glycoprotein (MOG) antibodies occur in a small group of neuromyelitis optica spectrum disorders. However, the clinical significance of this autoantibody has not been fully established. Case presentation An 18-year-old woman with a history of depression and atopic disease developed left-side dominant diffuse muscle weakness and numbness with bilateral ankle pseudoclonus along with deterioration of atopic dermatitis, which suggested the possibility of central nerve system damage, although there were no abnormal findings on magnetic resonance imaging. During hospitalization, her neurological symptoms naturally improved, so a wait-and-see approach was chosen. After discharge, she developed temporal blurred vision, and then a modest elevation in anti-MOG antibodies (1:128) was observed. We subsequently diagnosed the patient with possible anti-MOG antibody-associated disease. After intravenous methylprednisolone therapy was started, her pseudoclonus and gait disturbance were improved. Conclusions This case suggests that atopic dermatitis is possibly a trigger for developing anti-MOG antibody-associated disorder, and that some instances of possible central nerve system-demyelinating disease associated with anti-MOG antibodies could be poorly identifiable using magnetic resonance imaging. Anti-MOG antibody test might be worthwhile when a patient develops neurological symptoms without apparent magnetic resonance imaging lesions.

Transverse myelitis (TM) with systemic lupus erythematosus (SLE) has been linked to the presence of autoantibodies (eg, antiaquaporin 4 (AQP4) and anticardiolipin (aCL)) and SLE-induced secondary vasculitis, but the aetiology remains incompletely understood. A 48-year-old Japanese man with a 6-year history of poorly controlled SLE had stopped glucocorticoid therapy 1 year before admission. 3 days before admission, he developed flaccid paraplegia. Spinal MRI showed a longitudinally hyperintense T2 grey matter lesion from the level of Th4 to the conus medullaris, which was considered longitudinally extensive TM (LETM). We administered steroid pulse therapy (methyl-prednisolone 1000 mg/day) for 3 days and prednisolone 50 mg/day. The patient's flaccid paralysis gradually improved. We concluded that the patient's TM was caused by SLE flare-up, even though we could not completely rule out antiphospholipid syndrome. SLE myelitis is relatively rare and many aetiologies are possible for TM in SLE.