The symptoms of these diseases, which vary from one patient to another, can be so similar that NMOSD was once considered a variant of MS. Indeed, MS patients may experience sensory disturbances, muscle paralysis or weakness, and balance disorders (dizziness in particular), often associated with coordination problems. They may also experience visual impairment (reduced visual acuity possibly accompanied by pain around the orbit – particularly when the eye is in motion –, double vision, retrobulbar optic neuritis [inflammation of the optic nerve]), facial paralysis, speech and/or swallowing disorders, as well as bladder and sphincter control issues.
MS also progresses in the form of attacks, but unlike NMOSD, in which attacks are severe, with a high potential for disability from the very first episode, MS symptoms generally remit completely at the early stages of the disease.
Notably, optic neuritis is rarely severe in MS, unlike in patients with NMOSD. MS may also progress over time, whereas NMOSD does not progress between attacks, except in very rare cases.
The recent discovery of anti-aquaporin 4 (AQP4) antibodies in the blood of 70% of NMOSD patients has facilitated the differential diagnosis between these diseases. To date, no autoantibodies have been identified in MS. However, 30% of NMOSD patients have no anti-AQP4 antibodies in their blood, making the differential diagnosis more difficult. The combination of brain and spinal cord magnetic resonance imaging (MRI) findings, clinical signs and additional examinations (lumbar puncture, blood tests), helps to establish the differential diagnosis.
NMOSD and MS are now considered to be distinct diseases and require different therapeutic management approaches. These diseases must also be differentiated from MOG antibody-associated disease (MOGAD), acute disseminated encephalomyelitis (ADEM), or recurrent episodes of transverse myelitis or optic neuritis (ON).