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This study was initiated to examine the role of prostanoids (thromboxane) in the development of nutritional encephalomalacia (NE). Chicks were fed diets deficient in or supplemented with vitamin E in the presence or absence of a known prostaglandin inhibitor, acetylsalicylic acid (ASA). When the incidence of NE was approximately 50% in the vitamin E--deficient group without ASA supplement, the chicks were killed, and serum thromboxane B2 (TxB2) and serum and brain fatty acid (FA) composition were determined. The incidence of NE was not altered by ASA treatment. Plasma arachidonate levels were increased by ASA treatment on the vitamin E--deficient diet. Furthermore, the serum TxB2 levels in vitamin E--deficient versus vitamin E--adequate chicks, unlike changes noted for rats, were decreased. Aspirin treatment drastically reduced TxB2 levels in all groups but did not alter the incidence of NE. Therefore, it is unlikely that the development of NE is a result of thromboxane-mediated thrombosis.

At autopsy in the past three years, a new complex of CNS lesions has appeared in 54% (50/93) of the brains of premature infant cadavers that have come from our neonatal intensive care unit. This complex consists of necrotizing lesions in the periventricular white matter and in the gray nuclei of the cerebral hemispheres, the hippocampus and subiculum, cerebellar folia and white matter, and basis pontis. This entity is called the periventricular leukomalacia complex, since the distribution of lesions is similar, yet much more severe, than that described by Banker and Larroche in 1962. Clinical studies have indicated that these lesions may be related to long periods of time at high blood oxygen or prolonged periods in which PO2 and pH fluctuated widely.

The effect of high dietary sulfur (S) supplementation on blood thiamine (B1) concentration, biochemical indices of liver, muscle and kidney damage and selected plasma electrolytes was studied in six sheep. Three of these sheep received an additional 230 mg thiamine/kg diet (Group 2). After approximately 2.5-3 weeks on this diet, all three sheep in the non-B1-supplemented group (Group 1) showed loss of appetite and developed mild neurological signs: depression, intermittent signs of excitation and head pressing. Increases in blood B1 concentration and plasma creatine kinase (CK) and aspartate aminotransferase (AST) were observed during this time in all affected animals. Clinical signs lasted only for two to five days. Sheep in group 2 were clinically normal throughout the experiment, but all of these animals also had elevated blood B1 concentrations and plasma CK activity at the 3 wk sampling. Plasma magnesium concentrations of group 1 sheep were elevated at the 2.5-3 wk and 6 wk samplings but they declined significantly (p less than 0.05) to low normal levels thereafter. Magnesium concentrations of group 2 sheep were low at the beginning but progressively increased during the course of the experiment. At necropsy, brain lesions suggestive of polioencephalomalacia (PEM) were observed in all sheep but were most marked in group 1. It is speculated that PEM may be caused by a direct toxic effect of S, S metabolites or B1 antimetabolites in the brain rather than by an in vivo B1 deficiency per se.

Polioencephalomalacia (PEM), a disease first described in the United States and related to intensive beef production, appeared in Cuba coincident with the use of a new, molasses-urea-based diet to fatten bulls. Because the only experimental means so far of reproducing PEM has been with amprolium, a structural analog of thiamin, the present study attempted to induce the disease using the molasses-urea-based diet. Six Holstein bulls (200-300 kg) were studied during consumption of three successive diets: 1) commercial molasses-urea-restricted forage diet of Cuban feedlots, 2) a period in which forage was gradually withdrawn and 3) a forage-free diet composed only of molasses, urea and fish meal. PEM was reproduced in this way. At ten-day intervals, blood concentrations of glucose, lactate, pyruvate and urea were measured, as well as when clinical signs of PEM appeared. The signs, clinical course and lesions of the experimentally induced disease were comparable to those of field cases. The biochemical results suggested a block in pyruvate oxidation as in PEM elsewhere in the world. No evidence existed of urea intoxication. In addition, brain and liver concentration of total thiamin from field cases and normal animals were found to be similar.

Erythrocyte transketolase activity and the effect of adding thiamine pyrophosphate (% thiamine pyrophosphate effect) were measured in 111 subjects suspected to suffer from Leigh's disease (subacute necrotising encephalomyelopathy). From clinical evidence these subjects were divided into five groups: (1) necropsy-proved cases of subacute necrotising encephalomyelopathy, (2) cases positive for urinary thiamine pyrophosphate: adenosine triphosphate phosphotransferase inhibitor, (3) clinically likely cases of subacute necrotising encephalomyelopathy (patients still alive, or on whom no necropsy was performed), (4) cases diagnosed as diseases other than subacute necrotising encephalomyelopathy (control group), (5) cases for which no diagnosis had been made. Comparison of erythrocyte transketolase activities with and without added thiamine pyrophosphate and of the % thiamine pyrophosphate effect for each group compared with the control group showed no statistically significant differences from normal values for any of these parameters. Similarly, there were no differences between the two sexes in transketolase activity, and no correlation between transketolase activity and age. These results indicate that erythrocyte transketolase activity is not altered in subacute necrotising encephalomyelopathy and is unlikely to be of value for the diagnosis of Leigh's disease.

Thiamin concentrations were determined by the thiochrome method in blood from 16 cattle with polioencephalomalacia (PEM) or other apparent central nervous disorders. The mean blood total thiamin concentration of the five cattle with PEM (20.5 +/- 5.1 microg/100 ml blood) was not significantly different from concentrations in the cattle with the other disorders, despite evidence of a thiamin diphosphate deficiency reported in cattle with PEM.