Background

The presence of antibodies against the oligodendrocyte myelin glycoprotein (antiMOG-ab) is related to demyelinating disease of the central nervous system that especially affects the optic nerves (ON) and spinal cord (SC).

Objectives

Isolated and recurrent involvement of the SC without involvement of the ON is infrequent. More infrequently, this involvement occurs in the form of non-longitudinally extensive transverse myelitis (NLEMT).

Methods

We present two patients with the presence of antiMOG-ab and two episodes of NLEMT without ON involvement during the course of the disease.

Results

The first case is a 43-year-old man, with a history of pars planitis in childhood, who was admitted in March 2019 with lower limbs (LL) sensory symptoms and urinary sphincter disturbance of two weeks of evolution. Spinal magnetic resonance imaging (MRI) revealed an enhancing cord lesion at T4 level. The patient showed a positive determination of antiMOG-ab in serum. After treatment with methylprednisolone (MP) megadose, the patient recovered without sequelae. Chronic immunosuppression was not started after this first episode. In June 2020, symptoms compatible with a new transverse myelitis (TM) began. Complementary tests showed a new T9-T10 gadolinium (GD) enhancing lesion in MRI, and maintained antiMOG-ab positivity. It was treated with MP megadose with symptons resolution. Currently, the patient is receiving prednisone at a dose of 1mg/ kg and is pending the initiation of Rituximab.

The second case is a 48-year-old man, with no history of interest, who was admitted in November 2009 for symptoms of sensory disturbance and weakness in LL. The MRI study showed the presence of a GD enhancing lesion at C3 level and no additional alterations were observed by complementary tests. AntiMOG-ab was not determined. The patient improved after treatment with MP megadoses. Interpreted as idiopathic TM it remained asymptomatic until December 2019, when it started a clinical picture compatible with a Brown-Sequard syndrome. The spinal MRI revealed a new lesion at C6 level. On this occasion, a positive determination of antiMOG-ab was obtained in serum. It was treated with MP megadoses with almost complete resolution of the symptoms. Currently on Rituximab treatment with good response after six months.

In both patients, the first determination of anti MOG-ab was obtained using ELISA techniques in our hospital laboratory. These results were confirmed in an external laboratory using cell-based assay techniques.
In both cases, optical coherence tomography and evoked potentials were performed, which did not show alterations of ON.

Conclusions

In patients with recurrent NLEMT and no involvement of ON, a determination of antiMOG-ab should be performed as part of their evaluation.