Abstract
The spectra of myelin sheath thickness and g ratio (axon diameter/fibre diameter) of guinea pig optic nerves for 8 animals with acute experimental allergic encephalomyelitis (EAE) were compared with those for 6 normal animals. The mean myelin sheath thickness of 0.12 μm for the animals with EAE was significantly lower than the value of 0.16 μm for the normal animals. Since fibre diameter comprises axon diameter plus the thickness of its surrounding myelin sheath, a reduction in mean fibre diameter from 1.52 μm in normals to 1.20 μm in EAE was expected, but it was surprising to find that a mean g ratio of 0.85 obtained for normal nerves was not substantially different from a value of 0.86 for demyelinated optic nerves. A decrease in the mean axon diameter of 1.24 μm for normal animals to 0.94 μm for those with EAE tended to offset the decrease in mean myelin sheath thickness and contributed to the relative stability of the g ratio with acute demyelination. Our results showing reduction in axonal calibre and myelin sheath thickness may offer an explanation for apparent discrepancies between electrophysiological delays in conduction characteristics of experimental and, if not the result of a maturational effect on myelination, human primary demyelinating disorders associated with the scant histopathological demyelination of initial attacks of EAE and the visually asymptomatic patients with multiple sclerosis.
