Abstract

From a study of diphtheritic neuropathy in the guinea-pig, in which the clinical and electrophysiological findings have been correlated with the pathological changes at different stages of the disease, the following points emerge. 1. (1) Slight widening of the nodes of Ranvier preceded the onset of detectable functional disability; maximal velocity in motor fibres was not significantly reduced at this time. 2. (2) The profound fall in conduction velocity which occurred during a severe clinical illness was accompanied by myelin destruction involving complete internodal segments. Evidence is presented which indicates that the reduced velocity recorded at this time was not merely due to conduction block in the fastest conducting fibres. 3. (3) Whereas functional recovery was related to early remyelination of affected internodal segments, slow conduction persisted for several weeks after the clinical illness. The later recovery of conduction velocity was accompanied by a gradual increase in the thickness of the newly-formed myelin. 4. (4) The presence of axonal degeneration in a proportion of the fibres raises the possibility that loss of myelin may, under certain conditions, lead to destruction of the axon.

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