Sheep have been used to study the effect of dietary iodine deficiency on the development of the fetal brain. Severe iodine deficiency caused reduction in fetal brain and body weights and in brain DNA and protein from 70 days gestation to parturition. The lowered brain weight and brain DNA at 70 days gestation indicates a reduced number of cells, probably due to slower neuroblast multiplication which normally occurs from 40-80 days in the sheep, and the reduction in DNA and protein after 80 days implies that the development of neuroglia could be slowed also in iodine deficiency. Morphological changes were observed in both the cerebral hemispheres and the cerebellum. In the cerebral hemispheres of the iodine-deficient fetuses an increased density of neurons was apparent histologically in the motor cortex and visual cortex and in the CA1 and CA4 areas of the hippocampus in comparison with controls. In the cerebellum there was delayed migration of cells from the external granular layer to the internal granular layer and increased density of Purkinje cells in the iodine-deficient fetal brains. In addition, the molecular area was increased and the medullary area reduced in comparison with controls. These change are indicative of delayed brain maturation. Evidence of fetal hypothyroidism was provided by low fetal thyroid iodine and plasma T4 values, thyroid hyperplasia from 70 days gestation, significant reduction in body weight at the same time as the brain retardation, and absence of wool growth and delayed skeletal maturation near parturition. It is apparent from the biochemical and histological changes observed during iodine deficiency that iodine is an essential element for normal fetal brain and physical development in the sheep.
The combination of maternal and fetal thyroidectomy was found to have a significant influence on brain development in the fetal sheep at 140 days. There was reduced body weight (36%), brain weight (23%), DNA (26%) and protein (34%) content in five fetuses of ewes, subjected to thyroidectomy six weeks before mating and fetal thyroidectomy at 98 days gestation, compared with six sham operated controls. Cholesterol content was also reduced (36%) and water content increased (2.4%). The cerebellum was most severely affected and showed histologically an increased cell density associated with a significant reduction in the ratio of the molecular to granular cell layer area. The cell density was also significantly increased in the CA1 region of the hippocampus, but not in the CA4 region. It was also increased in the parietal layer of the cerebral cortex but not in the motor region. There was a significant reduction in the weight of heart (28.6%) and lungs (33.4%), while the kidneys and pituitary were enlarged (20.5% and 48.5% respectively) as a result of double thyroidectomy. The combined thyroidectomy was similar to iodine deficiency in its effect on fetal brain development, indicating that it is probable that iodine deficiency has its effects in the sheep by a combination of maternal and fetal hypothyroidism.
Merino ewes were surgically thyroidectomized, and mated 6 weeks later when their plasma thyroxine (T4) levels were negligible. Their foetuses were delivered by hysterotomy at 52, 71, 84, 98, 125, 140 days gestation or at term (150 days). Despite the very low levels of T4 in maternal plasma, the concentrations of T4 in foetal plasma were not significantly different after 71 days gestation from those of foetuses of sham\x=req-\ operated (control) ewes. Foetal brain and body weights, however, were reduced from 71 days compared to those of foetuses of sham-operated ewes. The foetal brain weights but not the body weights were restored to normal from 125 days to term. In additon to the weights, cell number (DNA) and cell size (protein:DNA ratio) appeared to be normal in the neonatal brain at parturition and this was confirmed by histological examination of the brains. Thus lack of maternal thyroid hormones in early pregnancy may cause a reduction in brain and body growth in the foetus which, in the case of the brain, appears to be restored to normal after the onset of foetal thyroid function.Man et al. (1971), in a study of the progeny of untreated hypothyroxinaemic women, have re¬ ported that at 7 years of age 36% of the offspring were found to be in the dull normal range men¬ tally compared to only 16% of the children of euthyroid mothers. As a result it has been postu¬ lated that the prenatal thyroid state of the mothers must be considered in the etiology of mental retardation in growing children.Furthermore, surgical thyroidectomy per¬ formed on foetal sheep during the third trimester of pregnancy (Mclntosh et al. 1979b) has demon¬ strated conclusively that an active supply of foetal thyroid hormone is essential for normal develop¬ ment of the sheep foetal brain 'in utero'. The thyroidectomized lambs at birth were charac¬ terised by reduced body weight, reduced wool growth, delayed skeletal maturation as well as retarded brain development which was estab¬ lished by reduced deoxyribonucleic acid (DNA), ribonucleic acid (RNA) and protein. The effects, particularly relating to the brain, were more severe when thyroidectomy was performed at 50-60 days of pregnancy . Iodine deficiency also has been shown to pro¬ duce adverse effects on the developing foetus and foetal brain (Potter et al. 1981 and, while the effects were not unlike those of foetal thyroid¬ ectomy, the retardation produced was much more severe in iodine deficiency. However, in support of the concept that the action of iodine in re¬ tarding foetal brain development is due only to its incorporation into the thyroid hormones, Mclntosh et al. (1983) showed that the foetal brain retardation after foetal thyroidectomy alone or in iodine deficiency was less severe than that caused by maternal thyroidectomy before conception fol¬ lowed by foetal thyroidectomy. It is likely then that, prior to the development of the foetal thy¬ roid and secretion of T4, embryonic brain and somatic growth could rely to a large extent on the availability of hormone supplied by th...
Urethral instability plays an essential role in the pathogenesis and progression of OAB in children. Synchro-cystourethrometry is a useful urodynamic technology to precisely diagnose OAB, and transcutaneous electrical pudendal nerve stimulation may be an effective treatment for OAB children induced by URI.
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