What histologic features characterize demyelinating diseases?

Study for the Histopathology and MTLE Test. Prepare with flashcards and multiple choice questions. Gain insights into the exam format, essential topics, and tips to excel your preparation!

Multiple Choice

What histologic features characterize demyelinating diseases?

Explanation:
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.

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