THE occurrence of distal degeneration or dying-back of long axons in a symmetrical polyneuropathy is usually interpreted as indicating that the primary metabolic disturbance is located within neurons rather than in myelin or in supporting structures in the nerve. Whether this particular pattern of neuronal degeneration is due to a diminished output from the perikaryon of some essential axonal metabolite or to a disturbance in axonal transport devices, or to some other mechanism is not known. It has recently been shown that the fine structure and the rate of flow of axoplasmic proteins in the peripheral nerves in experimental triortho-cresyl phosphate polyneuropathy and experimental acrylamide polyneuropathy1-3 are affected in different ways in these two dying-back polyneuropathies, and it would appear that more than one subcellular mechanism can lead to distal axonal degeneration. In the following report, the fine structural changes in the peripheral nervous system in thiamine hydrochloride-deficient