Article Text

Download PDFPDF
Bilateral frontal cortex encephalitis and paraparesis in a patient with anti-MOG antibodies
  1. Juichi Fujimori1,
  2. Yoshiki Takai2,
  3. Ichiro Nakashima2,
  4. Douglas Kazutoshi Sato2,
  5. Toshiyuki Takahashi2,3,
  6. Kimihiko Kaneko2,
  7. Shuhei Nishiyama2,
  8. Mika Watanabe4,
  9. Hiroaki Tanji1,
  10. Michiko Kobayashi1,
  11. Tatsuro Misu5,
  12. Masashi Aoki2,
  13. Kazuo Fujihara5
  1. 1 Department of Neurology, Tohoku Medical and Pharmaceutical University, Sendai, Japan
  2. 2 Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan
  3. 3 Department of Neurology, Yonezawa National hospital, Yonezawa, Japan
  4. 4 Department of Pathology, Tohoku University Hospital, Sendai, Japan
  5. 5 Department of Multiple Sclerosis Therapeutics, Tohoku University Graduate School of Medicine, Sendai, Japan
  1. Correspondence to Dr Juichi Fujimori, Department of Neurology, Tohoku Medical and Pharmaceutical University, 1-12-1 Fukumuro, Miyagino-ku, Sendai 983-8512, Japan; j-fujimori{at}

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Encephalitis seldom causes paraparesis as the initial symptom. Here, we report a case of steroid-responsive bilateral frontal cortical encephalitis involving leg motor areas in a patient who presented with paraparesis on admission. Interestingly, the initial paraparesis evolved into an acute disseminated encephalomyelitis (ADEM)-like illness and optic neuritis, and the patient was found to be positive for anti-myelin oligodendrocyte glycoprotein (MOG) antibodies.

Case report

A 46-year-old man experienced transient dizziness in early September 2008. Brain MRI retrospectively showed a slight fluid attenuation inversion recovery (FLAIR) high-intensity lesion involving the left frontal cortex (figure 1). One week later, the patient experienced a focal motor seizure in the right leg that subsequently generalised. Thereafter, he gradually developed headache and paraparesis over the course of a week. On admission, he presented with paraparesis without other neurological deficits, but the spinal MRI was normal. An electroencephalogram revealed that there were no epileptic discharges. A cerebrospinal fluid (CSF) examination revealed elevated leucocytes (56 /µL; 93% mononuclear cells, 3% polymorphonuclear leucocytes) and normal protein (36 mg/dL) and glucose (59 mg/dL) levels. The myelin basic protein (MBP) and glial fibrillary acidic protein levels in the CSF were not elevated. Cell-based assays for anti-N-methyl-D-aspartate receptor (NMDAR) antibodies, anti-voltage-gated potassium channel (VGKC) antibodies, anti-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) antibodies and anti-γ-aminobutyric acid-B receptor (GABA(B)R) antibodies in the CSF were negative. Blood and CSF examinations for infectious central nervous system (CNS) CNS diseases, collagen diseases, vasculitis, Behçet disease, sarcoidosis, lymphoma, paraneoplastic syndrome, vitamin B deficiency and Hashimoto encephalopathy were unremarkable.

Figure 1

Upper panel: axial fluid attenuation inversion recovery (FLAIR) images (1.5 T; TR 6000 ms, TE 105 ms). (A) Brain MRI at …

View Full Text