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Abstract
Observations have been made on 10 baboons receiving a high-dose regimen of clioquinol
administered orally, 6 receiving a low-dose regimen and 6 treated with 2,5-hexanedione.
The results were compared with those obtained from 10 control animals. Motor and sensory
nerve conduction velocity was markedly reduced in the hexanedione-treated animals
but only very minor abnormalities were detected in the clioquinol-treated baboons.
Cervical and Rolandic somatosensory evoked potentials to lower and upper limb stimulation
were delayed in both the high-dose clioquinol-treated and the hexanedione-treated
animals, particularly in the latter.
Histopathological studies in the low-dose clioquinol-treated group showed no abnormalities.
In the high-dose group; axonal degeneration was confined to the spinal cord, cerebellar
vermis and optic tract. It was most marked in the rostral portions of the dorsal spinal
columns and the caudal parts of the direct and crossed corticospinal tracts. Occasional
dorsal column fibres had degenerated back to the root entry zone in the cord. The
distribution was that of a selective central distal axonopathy. There appeared to
be no correlation with estimated blood levels of unaltered clioquinol. In hexanedione-treated
animals there was also degeneration in the distal optic tracts and peripheral nerves
in a pattern of central-peripheral distal axonopathy.
Keywords
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Article info
Publication history
Accepted:
February 3,
1984
Received:
January 13,
1984
Footnotes
☆This work was partly supported financially by the Friedreich's Ataxia Group.
Identification
Copyright
© 1984 Published by Elsevier Inc.
