MOGAD: How it differs from and resembles other neuroinflammatory disorders

Research output: Contribution to journalArticlepeer-review

Abstract

Myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD) is a distinct CNS inflammatory disease with symptoms and imaging findings that overlap other neuroinflammatory disorders. We highlight the imaging characteristics of MOGAD and contrast them with neuromyelitis optica spectrum disorder (NMOSD) and multiple sclerosis (MS). Intracranial features that suggest MOGAD include childhood acute disseminated encephalomyelitis pattern with diffuse signal abnormality in the cortical gray matter, subcortical white matter, deep white matter, and deep gray matter on T2-weighted and FLAIR images; few bilateral T2-hyperintense fluffy and poorly demarcated lesions; pontine or thalamic involvement (or both); and cerebellar peduncle lesions in children. Intraorbitally, one sees edematous, enlarged, tortuous optic nerve or nerves; bilateral long-segment T2 hyperintensity of anterior segments of the optic nerve; sparing of the optic chiasm and retrochiasmatic pathways; and perioptic nerve sheath and surrounding orbital fat enhancement. Spinal involvement is seen as longitudinally extensive transverse myelitis with a sagittal T2-hyperintense intramedullary spinal line, the axial “H” spinal cord sign (central cord gray matter T2 hyperintensity), and conus medullaris involvement. Early accurate diagnosis of MOGAD is important because prognosis and treatment differ from those for NMOSD and MS.

Original languageEnglish (US)
Pages (from-to)1031-1039
Number of pages9
JournalAmerican Journal of Roentgenology
Volume216
Issue number4
DOIs
StatePublished - Apr 2021

Keywords

  • Brain
  • MOGAD
  • MRI
  • Multiple sclerosis
  • Myelin oligodendrocyte glycoprotein antibody–associated disease
  • Neuromyelitis optica spectrum disorder
  • Orbit
  • Spine

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging

Fingerprint Dive into the research topics of 'MOGAD: How it differs from and resembles other neuroinflammatory disorders'. Together they form a unique fingerprint.

Cite this