Evidence for subacute fat embolism as the cause of multiple sclerosis.

The neurological features of decompression sickness, which is thought to be due to gas embolism, are similar to those of multiple sclerosis (MS). This similarity suggested the re-examination of a concept, first proposed in 1882, that the demyelination in MS is due to venous thrombosis. Unfortunately, although the plaques of MS are often perivenular, thromboses are not always present. Nevertheless, vascular theories can explain the topography of the lesions in MS. Embolism is generally associated with arterial rather than venous damage, and with neuronal infarction rather than loss of myelin. However, the intra-arterial injection of a range of substances can cause venous damage and perivenous demyelination in the brain, although it does not exactly reproduce the plaques seen in man. There is also evidence in man that fat may lodge in the microcirculation of the nervous system and cause distal perivenous oedema with the loss of myelin from axons. Since acute fat embolism may produce lesions not only in the white matter of the brain, but also in the cord, the retina, the meninges, and the skin, and since all these have been described in MS, subacute fat embolism may be the cause of MS.