The Spanish toxic-oil syndrome: three years of evolution.

In a recent issue of Muscle k? Nenle, Vallat et al." concluded as have ot.her authors before,' that peripheral nerve involvernetit in the toxic syndrome is attributable to factors other than a direct action of a putative neurotoxin. Our electrophysiologic study' of the disease within the first year of evolution suggests that the neuromuscular impairment is a slowly progressive mixed axonal neuropathy, asymmetric in some patients, which is in accordance with the neuropathologic findings encountered of mixed ischemic and fibrotic changes in the n e r ~ e . ' ~ ' I * ~ ~ ' ~ Nevertheless, the exact ethiopathologic mechanisnis are as yet unknown. We have not attempted to defend one or more of the hypotheses that have been put forward.' Several authors'.' have stated that the anilides of fatty acids are not an impor&irit lacmiin the toxic-oil mixture, hut other^^*".('*'^ seem to have reproduced with them some similar changes in animal models. The WHO commissionIg has drawn some of the following conclusions in this respect. It seems reasonable to state that there are toxic mechanisms in the initial acute phase of the illness, with transient allergic features superimposed. The pathogenesis apparently affects the endothelial system, involving the lung severely in the initial phase. The mechanisms involved in the chronic phase have not as yet been established, although direct toxicity and/or autoimmune responses may play a role. Attempts to reproduce the condition in animal models have had variable results. The reasons for this may he explained by the lack of an appropriate animal model, difficulties in the design of the experimental work, inadequate histologic sampling and/or probably the lack of recognition of other nutritional factors that might have favored the occurrence of the syrirli.oine, and last, but not least, the lack o f coordination between different groups o f scientists. The electrophysiologic findings in 145 patients within the first year of evolution were reported in our previous article.' The results of the study in 64 new cases and the follow-up in 14 patients 12-36 months after onset of intoxication were in agreemcnt with those previously reported.' In general, conduction velocity improved and signs of progressive reinnervation were found in the course of evolution o t the patients with mild to severe neurornuscular impairment. However, some ci~scs wir.h severe disability remained with complete or nearly tol.al denervation in distal hrib muscles, and sensory potentials could be absent. These patients showed very slow improvement with rehabilitation therapy and still present severe muscle atrophy, paresis, and joints limitation. These findings suggest that the disease has entered in a chronic phase. Six patients with only slight or mild electrophysiologic changes developed a typical bilateral carpal tunnel syndrome. Perincural fibrosis, reported in the previous articles,'.p may play a role in the nerve entrapment. SFEMG showed that collateral reinnervation with rearrangement of fibers within the motor unit was a striking finding in patients with high grade of disability (Table 1). Fiber density of the motor unit was higher in