Brain and spinal cord scars in people with multiple sclerosis (MS) may reveal why they develop progressive disabilities, research suggests.
A new study explores whether inflammation leads to permanent scarring in three diseases. Researchers examined multiple Sclerosis (MS), Aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4-NMOSD) and Myelin oligodendrocyte glycoprotein antibody-associated disorder (MOGAD).
They also assessed if the scarring offers a reason for the absence of slow progressive disability in AQP4-NMOSD and MOGAD.
Damage and repair
The body’s immune system targets the myelin, the insulation around the nerves in all three conditions. This causes inflammation and leads to the removal of the myelin within the brain and spinal cord. Areas of demyelination appear as white spots on an MRI.
This could lead to symptoms such as visual problems, numbness, weakness, bowel or bladder dysfunction.
The repair mechanisms within the body try to reinstate the nerves and repair the lesions but this can be incomplete. It could result in a scar that remains visible on MRIs and leaves nerve fibres vulnerable to further damage over time.
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Multiple sclerosis study
The study, published in the Neurology Journal, included 156 patients: 67 had MS, 51 had AQP4-NMOSD and 38 had MOGAD. The patients had suffered 172 attacks or relapses combined.
The researchers revealed that with MS, areas of inflammation reduced only modestly in size which led to a moderately sized scar. If the scar is in a region of the brain and spinal cord that controls arm or leg muscles then nerve fibres can degenerate and cause slow worsening of the disability in the secondary progressive course of MS.
Research and results
Eoin Flanagan, a Mayo Clinic neurologist and senior author of the study said: “The differences in scarring that we found will help physicians distinguish these three diseases more easily to aid in diagnosis.
“More importantly, our findings improve our understanding of the mechanisms of nerve damage in these three diseases and may suggest an important role of such scars in the development of long-term disability in MS.”
AQP4-NMOSD and MOGAD do not share the same slow progression of disability that MS does.
With AQP4-NMOSD, large areas of inflammation occur during attacks causing severe symptoms. Scarring is common but smaller than and in less important locations than MS. This leads to fewer long-term problems.
Researchers found that with MODGAD, despite the large areas of inflammation that occur during an attack, the lesions tend to disappear completely over time.
With MOGAD, despite having large areas of inflammation during an attack, the researchers found lesions tended to disappear completely over time and not leave any scar. This fits well with the excellent recovery from episodes and overall good long-term prognosis without the slow worsening disability seen in MS.
Future study
While the reasons for the recovery are not known, it could mean an enhanced ability to put the covering back onto nerves.
Dr Flanagan concluded: “We hope that the improved understanding on the ways MOGAD repairs its lesions so well may lead to novel treatment avenues to prevent scar formation in MS.”
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