General description

Anti-MOG antibody-associated disease (MOGAD) is an inflammatory demyelinating disorder of the central nervous system, affecting the brain, spinal cord, and optic nerves. It is caused by autoantibodies targeting myelin oligodendrocyte glycoprotein (MOG). MOGAD encompasses a spectrum of diseases with diverse neurological manifestations, including Neuromyelitis optica spectrum disorder (NMOSD), transverse myelitis, Acute disseminated encephalomyelitis (ADEM), brainstem inflammation, and cortical encephalitis.

MOGAD was initially identified as a subgroup of Neuromyelitis optica spectrum disorder (NMOSD) characterized by the presence of anti-MOG antibodies and the absence of anti-AQP4 antibodies. It was later recognized as a distinct and independent disease entity, separate from NMOSD.

The symptoms of MOGAD vary depending on the site of inflammation and demyelination. Key symptoms include:

• Optic neuritis: Vision loss, visual field defects, and eye pain, which may affect one or both eyes.
• Acute disseminated encephalomyelitis (ADEM): Loss of consciousness, abnormal behavior, fever, seizures, motor dysfunction (e.g., paralysis of the arms and legs), and ataxia.
• Transverse myelitis: Motor and sensory disturbances, as well as bladder and bowel dysfunction.
• Cortical encephalitis: Characterized by convulsive seizures, with MRI revealing cortical lesions.

Diagnosis of MOGAD is based on neurological examination, MRI, cerebrospinal fluid analysis, and testing for anti-MOG antibodies. The presence of anti-MOG antibodies in the blood or cerebrospinal fluid, especially in the absence of aquaporin-4 (AQP4) antibodies, confirms the diagnosis of MOGAD. MOGAD is now recognized as a distinct disease entity, separate from Neuromyelitis optica spectrum disorder (NMOSD). In differential diagnosis, anti-MOG antibodies are typically absent in cases of Multiple sclerosis (MS).

In NMOSD, the concentration of glial fibrillary acidic protein (GFAP) in the cerebrospinal fluid is elevated due to damage to astrocytes. Conversely, the concentration of myelin basic protein (MBP) does not increase in NMOSD.
Conversely, in MOGAD, the damage to the myelin sheath leads to an increase in MBP levels in the cerebrospinal fluid, while GFAP levels remain unaffected.