MRI features of extraocular muscle metastases compared to those of other extraocular muscle diseases of non-thyroid origin.

AIM: To identify the magnetic resonance imaging (MRI) features of metastases to the extraocular muscles (EOM metastases). MATERIAL AND METHODS: The MRI features of 19 patients with EOM metastases were compared with those of 24 patients with EOM diseases of non-thyroid origin. MRI was used to assess the number of tumours, morphology, signal intensity on T2-weighted images, enhancement patterns, and apparent diffusion coefficient (ADC) values. RESULTS: Single muscular involvement was observed in 10 patients, and multiple muscular involvement was observed in nine patients. The morphology was focally discrete in nine patients, and diffuse infiltrative in 10 patients; all the nine patients with focal discrete morphology presented with single muscular lesions. On T2-weighted images, the signal intensities were intermediate or low in 15 patients and a mixture of high and intermediate in four patients. In 14 patients for whom contrast-enhanced images were available, ring enhancement (n=5), heterogeneous diffuse enhancement (n=5), and homogeneous enhancement (n=4) were seen. The mean ADC value was 0.98 × 10-3 mm2/s. Compared to other EOM diseases of non-thyroid origin, single muscular presentation, focal discrete morphology, the presence of hyperintensity on T2-weighted images, and ring or heterogeneous enhancement were significantly more frequent in EOM metastases. CONCLUSION: The MRI features of EOM metastases showed two main patterns: a single discrete mass and multiple infiltrative masses. In addition to the presentation as a single discrete mass, the presence of hyperintensity on T2-weighted images and ring or heterogeneous enhancement can aid in the differentiation of EOM metastases from other EOM diseases.

Acceleration of hypertensive cerebral injury by the inhibition of xanthine-xanthine oxidase system in stroke-prone spontaneously hypertensive rats.

It is well-known that, in ischemic cerebral injury, a free radical and its byproducts are generated by xanthine-xanthine oxidase system and eliminated by scavengers such as superoxide dismutase (SOD), catalase, uric acid and ascorbic acid. To investigate the possible involvement of the xanthine-xanthine oxidase system in hypertensive cerebral injury, we examined chronological changes in uric acid level in the cerebral cortex and the effects of the inhibition of xanthine oxidase or catalase using stroke-prone spontaneously hypertensive rats (SHRSP). In young SHRSP, uric acid content was lower than age-matched Wistar-Kyoto rats (WKY), but in mature SHRSP strongly exposed to oxidative stress uric acid content had risen dramatically. Administration of allopurinol, an inhibitor of xanthine oxidase, caused a marked decrease in uric acid content. In these SHRSP, cerebral injury was much more intense compared to the control group. On the other hand, administration of aminotriazole, an inhibitor of catalase, did not affect the brain pathology of SHRSP, in spite of a mild reduction in tissue uric acid content. These results suggest that the xanthine-xanthine oxidase system is not the major source of free radical generation in hypertensive cerebral injury. Moreover, the results also suggest that tissue uric acid may have a key role for the incidence of hypertensive cerebral injury in SHRSP.

Mitochondrial abnormalities in hypertrophied myocardium of stroke-prone spontaneously hypertensive rats.

1. To clarify the pathogenesis of cardiac disorders in SHRSP which showed severe cardiac hypertrophy and myocardial degeneration in the hypertensive stage, restriction fragment length polymorphisms (RFLP) of mitochondrial DNA (mtDNA), and morphological and functional changes of mitochondria were examined. 2. Morphologically, the mitochondrial size showed a wider range of distribution in SHRSP both at prehypertensive and hypertensive stage compared to those in age-matched WKY. 3. Isocitrate dehydrogenase (ICDH) activity, but not superoxide dismutase (SOD) activity, was higher in the young SHRSP, whereas both enzyme activities were lower in the mature SHRSP than in the age-matched WKY. 4. RFLP analysis by electrophoresis revealed that the loss of two restriction sites for Rsa I in the myocardial mtDNA from the SHRSP, but not in that from the WKY. 5. These findings suggest that the structural changes of mtDNA could be related, at least partly, to morphological and functional changes of mitochondria in the SHRSP myocardium.