TY - JOUR
T1 - Lead neuropathy
T2 - 2.Random distribution of segmental demyelination among “old internodes ” of myelinated fibers
AU - Dyck, Peter James
AU - O’brien, Peter C.
AU - Ohnishi, Akio
PY - 1977/1/1
Y1 - 1977/1/1
N2 - 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 internodesform following internodal segmental demyelination, of one “old internode” the lattermethod 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.
AB - 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 internodesform following internodal segmental demyelination, of one “old internode” the lattermethod 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.
UR - http://www.scopus.com/inward/record.url?scp=0017626099&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0017626099&partnerID=8YFLogxK
U2 - 10.1097/00005072-197705000-00014
DO - 10.1097/00005072-197705000-00014
M3 - Article
C2 - 871324
AN - SCOPUS:0017626099
VL - 36
SP - 570
EP - 575
JO - Journal of neuropathology and experimental neurology
JF - Journal of neuropathology and experimental neurology
SN - 0022-3069
IS - 3
ER -