Biopsies of muscle and sural nerves, and autopsies of patients affected by the toxic and neuromuscular syndrome produced by ingestion of adulterated rapeseed oil were studied using morphological, histochemical and ultrastructural methods. In muscle, two pathological pictures were distinguished according to their temporal sequence. In the early phase, the neuromuscular syndrome was characterized by myalgia and an inflammatory infiltration of the perimysium, the capsules of muscle spindles and intramuscular nerves. The muscle fibres exhibited small subsarcolemmal zones of fibril disintegration and accumulation of electron-dense material similar to Z bands. Areas of peroxidase activity were found in relation to the surface of many muscle fibres. In late stages there was severe neurogenic atrophy of muscle with intense endomysial fibrosis. Minimal perivascular inflammation by round cells, with no interstitial infiltrates, was finally present. The inflammatory myopathy that initially affected these patients differs from other forms of polymyositis and seems to be related to the inflammation present in other systems. The onset of denervation atrophy is secondary to the involvement of peripheral nerves which is the most salient and distinctive pathological feature of the syndrome. The involvement of peripheral nerves was the most severe pathological feature. Perineuritis and, later, fibrosis of the perineurium were conspicuous and peculiar to this toxic syndrome. Degeneration of myelinated axons was constant in late stages. Distal nerves were more affected than proximal nerves. In the CNS, chromatolysis of anterior horn cells and occasionally of cranial nerve nuclei, pontine nuclei and reticular neurons was found. In the brainstem, astrocytes were hypertrophic with abnormal nuclei and there was microglial proliferation in zones where chromatolysis was found. The possibility that free radicals derived from the adulterated oil and cytotoxic complexes formed by mast-cell granules and eosinophil peroxidases might have been involved in the pathogenesis is discussed. The toxic oil was rich in linoleic acid which, by forming an excess of arachidonic acid, might have played an additional role in the pathogenesis of the lesions.