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[Diphtheritic polyneuropathy: clinico-morphologic study]

S M Lozhnikova, V N Pirogov, M A Piradov

    Arkhiv Patologii
    |March 1, 1997
    PubMed
    Summary

    Grave Diphtheria-associated polyneuropathy (DP) involves toxic myelopathy and demyelination, particularly in large nerve fibers. Schwann cell activation and attempted remyelination occur, but recovery is incomplete even after 69 days.

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    Area of Science:

    • Neurology
    • Pathology
    • Cell Biology

    Background:

    • Diphtheria-associated polyneuropathy (DP) is a severe neurological complication.
    • Understanding the underlying pathology is crucial for patient management.

    Purpose of the Study:

    • To investigate the morphological changes in nerve biopsies from patients with severe DP.
    • To elucidate the mechanisms of demyelination and remyelination in DP.

    Main Methods:

    • Light and electron microscopy of sural nerve biopsies.
    • Analysis of biopsies from 18 patients at various disease stages (19-69 days).

    Main Results:

    • Toxic myelopathy with paranodal demyelination in large myelinated fibers and segmental demyelination in smaller fibers.

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  • Secondary axonal degeneration observed in severe cases due to myelin folding and Schwann cell invagination.
  • Absence of inflammatory cell involvement.
  • Significant Schwann cell proliferation and activation, indicating active myelin degradation and attempted remyelination.
  • Morphological evidence of remyelination by day 35, despite worsening neurological symptoms.
  • Incomplete remyelination observed even by day 69.

    • Conclusions:

    • Severe DP is characterized by toxic myelopathy and demyelination, not inflammation.
    • Schwann cell activity suggests a regenerative response, but remyelination is slow and incomplete.
    • The findings highlight the challenges in recovery from severe Diphtheria-associated polyneuropathy.