Study design: Double blind, partial crossover. Objectives: To evaluate the analgesic activity of a novel cranial electrostimulus in people with spinal cord injury (SCI). Setting: Hereward College, a residential centre that provides educational facilities for students with disabilities. Methods: Subjects with SCI experiencing chronic pain were randomly assigned into two groups, one of which received sham and the other transcranial electrostimulation treatment (TCET) on two occasions daily for four successive days. After a`wash-out' period of 8 weeks all subjects returned and received the identical stimulus that the treated cohort received on the ®rst arm of the study. Results: Pain measurements applied before and after each session indicated that the pain decreased in the treated group to 51% of that reported at the commencement of treatment; reported pain intensity did not decrease signi®cantly in the sham treated subjects. The same (sham) subject group reported experiencing 59% of the pain at the end of the second arm of the study (TCET) as on the ®rst arm (sham). No signi®cant di erences were determined between the mood of all subjects estimated before and after each sham or TCET treatment session. The reported analgesic, and combined antidepressant and anxiolytic drug use in subjects receiving TCET on the second arm of the study, was 46% and 53% respectively of the average pre-study drug use. No similar decrease in the use of the drugs was noted in the same subjects after sham treatment on the ®rst arm of the study. Salivary cortisol determinations made prior to and after each sham and treatment session implicated this corticoid in the pain-relieving mode of action of the treatment, but could not be associated with any changes in mood. Subjects receiving TCET had signi®cantly higher urinary 3-methoxy-4-hydroxy-phenylglycol (MHPG) output after the TCET treatment period than sham stimulation, implicating increased central noradrenaline (NA) metabolism in the observed e ects. Conclusion: The subjects reported less pain during, and immediately after receiving this transcranial treatment, although they were using less medication than when receiving sham treatment.
The concentration of lipoperoxides (estimated as thiobarbituric acid-reactive material) and some components of the antioxidant defence system have been compared in various tissues of lean and congenitally obese mice. NADPH-stimulated lipoperoxide generation in vitro was significantly higher in microsomes (microsomal fractions) prepared from obese hepatic tissue than lean. Plasma, liver and brain lipoperoxide concentration was significantly higher in obese mice. In blood derived from obese mice the concentration of non-enzymic antioxidants including caeruloplasmin and vitamin A was higher, but hepatic retinol concentration was lower in these animals. In all the tissues assayed the glutathione peroxidase activity against H2O2 was less than its activity against cumene hydroperoxide. Assayed with either substrate, glutathione peroxidase activity was significantly higher in the brain and blood of obese mice than their lean counterparts. Conversely, liver glutathione peroxidase was decreased in obese animals, representing 43% of the activity of the lean-mouse liver enzyme against H2O2 and 81% of the cumene hydroperoxide-reducing activity. The liver of obese mice had significantly less, and the kidneys more, oxidized glutathione than the corresponding tissues of lean mice. Further investigations on hepatic tissue indicated that glutathione reductase activity was lower in the obese animals, but there was no significant difference between glucose-6-phosphate dehydrogenase activity in obese and lean mice.
Rats of various ages were subjected to stress by confinement in restraining cages at 2-4 degrees C. Analysis of the plasma of these animals revealed an elevation in corticosteroids of approximately 50% above the control level. The livers of all the groups of cold-restrained animals contained significantly more lipoperoxide (estimated as thiobarbituric-acid-reactive material) than did control hepatic tissue. The plasma of the 12-, 24-, and 32-wk-old groups of rats subjected to stressful treatment also contained significantly higher lipoperoxide levels. There was no significant difference between the lipoperoxide levels of the brain tissue of control or stress-treated rats. The activities of both glutathione peroxidase and glutathione reductase were increased in hepatic, but not brain, tissue of the stressed animals. The perturbation of the activities of these enzymes did not produce any significant change in the ratio of reduced, oxidized glutathione. The livers of the stressed animals had significantly less total glutathione than those of the controls.
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