THE CHOROID PLEXUS IN PASSIVE SERUM SICKNESS

Abstract

One-hundred teased fibers of proximal and of distal sural nerve of five rats fed lead carbonate for 3 months were evaluated to see whether the pattern of segmental demyelination was random or clustered. If the evaluation was done by the length of the “territory of an old internode” (the region of one Schwann cell) a significant departure from randomness could not be shown for the majority of nerves. However, if the evaluation was by regions with and without myelin a highly clustered pattern of segmental demyelination was found. Since several remyelinated internodes form following internodal segmental demyelination, of one “old internode” the latter method of analysis would be expected to show clustering even though Schwann cell damage was random. Therefore the second method of analysis cannot be used to assess randomness of Schwann cell involvement in neuropathy. We interpret these studies as supporting the concept that Schwann cells are primarily and ubiquitously involved in lead neuropathy of the rat. Possible mechanisms of such primary Schwann cell injury are direct damage from lead of the intrafascicular interstitial fluid or from increased intrafascicular interstitial pressure.