What histologic features characterize demyelinating diseases?

What histologic features characterize demyelinating diseases?

• A. Perivascular inflammatory infiltrates with demyelination, relative axonal preservation early, and lipid-laden macrophages.
• B. Chronic gliosis without demyelination.
• C. Necrotic plaques with amyloid deposition.
• D. Granulomatous inflammation with multinucleated giant cells.

Answer: (A)

Immune-mediated loss of myelin around small blood vessels with active removal of myelin is the hallmark. In these demyelinating lesions you see perivascular inflammatory infiltrates—often around small veins and venules—with inflammatory cells like T cells and macrophages. The myelin sheaths are stripped from the underlying axons, yet the axons themselves are relatively preserved in the early stages. As myelin is degraded, macrophages ingest the myelin debris and become lipid-laden, giving a foamy appearance that highlights active demyelination. Over time, gliosis develops as part of scarring, but the key early combination is perivascular inflammation, demyelination with preserved axons, and lipid-laden macrophages. This pattern fits demyelinating diseases such as multiple sclerosis. Other patterns—gliosis without demyelination, necrotic plaques with amyloid, or granulomatous inflammation with multinucleated giant cells—point to different processes and do not match the typical demyelinating pathology.

Immune-mediated loss of myelin around small blood vessels with active removal of myelin is the hallmark. In these demyelinating lesions you see perivascular inflammatory infiltrates—often around small veins and venules—with inflammatory cells like T cells and macrophages. The myelin sheaths are stripped from the underlying axons, yet the axons themselves are relatively preserved in the early stages. As myelin is degraded, macrophages ingest the myelin debris and become lipid-laden, giving a foamy appearance that highlights active demyelination. Over time, gliosis develops as part of scarring, but the key early combination is perivascular inflammation, demyelination with preserved axons, and lipid-laden macrophages. This pattern fits demyelinating diseases such as multiple sclerosis. Other patterns—gliosis without demyelination, necrotic plaques with amyloid, or granulomatous inflammation with multinucleated giant cells—point to different processes and do not match the typical demyelinating pathology.