Facilitating Knowledge of Women on Importance of Iodine in Foetal Brain Development through Nursing Education: An Evidence-Based Educational Intervention

The purpose of the evidence-based practice educational intervention was to a) assess the knowledge of women on the importance of iodine in fetal brain development b) find the effectiveness of planned teaching program on women. Iodine Deficiency Disorders can impact on people of all ages, but most severely on the baby while it is developing in the womb. During pregnancy, it can cause maternal and fetal hypothyroidism and impair neurological development of the fetus. This study showed that women did not have enough knowledge regarding the importance of iodine in fetal brain development. So there was lack of knowledge in some aspects regarding the importance of iodine in fetal brain development among women residing in the rural area The nurses have an influential role in imparting knowledge on the importance of iodine in fetal brain development. They can utilize their opportunities to spread awareness about the importance of iodine deficiency disorders leading to brain damage. Providing EBP educational intervention on this topic positively impacted on their knowledge. The findings underscore evidence-based nursing is one approach that may enable future healthcare providers to manage the explosion of new literature and technology and ultimately may result in improved patient outcomes. Hence it helps to implement in their caregiving as a nurse educator, midwife, and as public health nurse.

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RETARDED FETAL BRAIN DEVELOPMENT RESULTING FROM SEVERE DIETARY IODINE DEFICIENCY IN SHEEP

Neuropathology and Applied Neurobiology ◽

10.1111/j.1365-2990.1982.tb00299.x ◽

1982 ◽

Vol 8 (4) ◽

pp. 303-313 ◽

Cited By ~ 54

Author(s):

B. J. POTTER ◽

M. T. MANO ◽

G. B. BELLING ◽

G. H. McINTOSH ◽

C. HUA ◽

...

Keyword(s):

Brain Development ◽

Iodine Deficiency ◽

Fetal Brain ◽

Fetal Brain Development

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The effect of thyroxine, 3,5-dimethyl-3'-isopropyl-L-thyronine and iodized oil on fetal brain development in the iodine-deficient sheep

Acta Endocrinologica ◽

10.1530/acta.0.1210007 ◽

1989 ◽

Vol 121 (1) ◽

pp. 7-15 ◽

Cited By ~ 6

Author(s):

M. T. Mano ◽

B.J. Potter ◽

G. B. Belling ◽

D. M. Martin ◽

B. G. Gragg ◽

...

Keyword(s):

Brain Development ◽

Thyroid Function ◽

Iodine Deficiency ◽

Fetal Brain ◽

Maternal Plasma ◽

Iodized Oil ◽

Irreversible Damage ◽

Fetal Plasma ◽

Fetal Brain Development ◽

Fetal Thyroid

Abstract. Studies have been carried out to investigate the role of maternal and fetal thyroid function in the effects of iodine deficiency on fetal brain development in sheep. Iodine deficiency was established with an especially prepared low-iodine diet of maize and pea pollard. The iodine-deficient sheep were mated and at the end of the second trimester of pregnancy (100 days gestation) were divided into groups which received either a sc injection of T4 or 3,5-dimethyl-3'-isopropyl-L-thyronine or an im injection of iodized oil. At 140 days gestation (10 days prior to parturition) comparison of the fetuses delivered by hysterotomy revealed that the retarded fetal brain development observed in iodine deficiency was greatly improved by T4 and by iodized oil. However, T4 and iodized oil failed to correct the reduction in the number and the increase in the length of synaptic appositions which were observed in the fetal cerebral cortex after iodine deficiency. In addition, the histological appearance of the fetal thyroid gland and the levels of plasma thyroid hormones were restored to normal. The administration of 3,5-dimethyl-3'-isopropyl-L-thyronine had no effect on the retarded fetal brain and body development of the iodine-deficient fetuses. The lack of response may be due to the inability of 3,5-dimethyl-3'-isopropyl-L-thyronine to cross the ovine placenta as no reduction in the abnormally elevated fetal plasma TSH was observed in spite of a fall in maternal plasma TSH and apparent restoration of maternal thyroid function. It is concluded that the retarded fetal brain development observed during iodine deficiency in sheep can be substantially improved by iodized oil or to a lesser extent by T4 administration at 100 days gestation and that this is dependent on the restoration of both maternal and fetal thyroid function which supports previous observations from this laboratory following fetal and maternal thyroidectomy. The persistence of some effects of iodine deficiency on the fetal brain suggests that irreversible damage may have occurred.

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Fetal brain development in response to iodine deficiency in a primate model (Callithrix jacchus jacchus)

Journal of the Neurological Sciences ◽

10.1016/0022-510x(87)90236-x ◽

1987 ◽

Vol 79 (3) ◽

pp. 287-300 ◽

Cited By ~ 28

Author(s):

M.T. Mano ◽

B.J. Potter ◽

G.B. Belling ◽

J. Chavadej ◽

B.S. Hetzel

Keyword(s):

Brain Development ◽

Iodine Deficiency ◽

Fetal Brain ◽

Callithrix Jacchus ◽

Primate Model ◽

Fetal Brain Development ◽

Callithrix Jacchus Jacchus

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New normal range of fetal cavum septum pellucidum in the second trimester of gestation

10.21516/2413-1458-2020-19-1-21-24 ◽

2020 ◽

Author(s):

M.V. Medvedev, O.I. Kozlova, À.Yu. Romanova

Keyword(s):

Brain Development ◽

Reference Range ◽

Fetal Brain ◽

Septum Pellucidum ◽

Second Trimester ◽

Normal Range ◽

Cavum Septum Pellucidum ◽

New Normal ◽

Biparietal Diameter ◽

Fetal Brain Development

Fetal brain was retrospectively evaluated in 418 normal fetuses at 16–28 weeks of gestation. The multiplanar mode to obtain the axial cerebral plane and measured the width of the cavum septum pellucidum (CSP) and biparietal diameter (BD). All measurements of CSP were done from as the widest diameter across both borders in an inter-to inter fashion. The CSP width is increasing at second trimester of gestation. Normal range plotted on the reference range (mean, 5th and 95th percentiles) of fetal width CSP by measuring of its size may be useful for assessment of fetal brain development in the second trimester of gestation.

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CB1 antagonism increases excitatory synaptogenesis in a cortical spheroid model of fetal brain development

Scientific Reports ◽

10.1038/s41598-021-88750-2 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Alexis Papariello ◽

David Taylor ◽

Ken Soderstrom ◽

Karen Litwa

Keyword(s):

Brain Development ◽

Spontaneous Activity ◽

Microelectrode Array ◽

Cannabinoid Receptor ◽

Fetal Brain ◽

Endocannabinoid System ◽

Autism Spectrum ◽

Nervous System Development ◽

Inhibitory Synapses ◽

Fetal Brain Development

AbstractThe endocannabinoid system (ECS) plays a complex role in the development of neural circuitry during fetal brain development. The cannabinoid receptor type 1 (CB1) controls synaptic strength at both excitatory and inhibitory synapses and thus contributes to the balance of excitatory and inhibitory signaling. Imbalances in the ratio of excitatory to inhibitory synapses have been implicated in various neuropsychiatric disorders associated with dysregulated central nervous system development including autism spectrum disorder, epilepsy, and schizophrenia. The role of CB1 in human brain development has been difficult to study but advances in induced pluripotent stem cell technology have allowed us to model the fetal brain environment. Cortical spheroids resemble the cortex of the dorsal telencephalon during mid-fetal gestation and possess functional synapses, spontaneous activity, an astrocyte population, and pseudo-laminar organization. We first characterized the ECS using STORM microscopy and observed synaptic localization of components similar to that which is observed in the fetal brain. Next, using the CB1-selective antagonist SR141716A, we observed an increase in excitatory, and to a lesser extent, inhibitory synaptogenesis as measured by confocal image analysis. Further, CB1 antagonism increased the variability of spontaneous activity within developing neural networks, as measured by microelectrode array. Overall, we have established that cortical spheroids express ECS components and are thus a useful model for exploring endocannabinoid mediation of childhood neuropsychiatric disease.

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Neuroplacentology in congenital heart disease: placental connections to neurodevelopmental outcomes

Pediatric Research ◽

10.1038/s41390-021-01521-7 ◽

2021 ◽

Author(s):

Rachel L. Leon ◽

Imran N. Mir ◽

Christina L. Herrera ◽

Kavita Sharma ◽

Catherine Y. Spong ◽

...

Keyword(s):

Brain Development ◽

Congenital Heart ◽

Fetal Brain ◽

In Utero ◽

Structure And Function ◽

Brain Growth ◽

Neurodevelopmental Outcomes ◽

Fetal Brain Development ◽

And Function

Abstract Children with congenital heart disease (CHD) are living longer due to effective medical and surgical management. However, the majority have neurodevelopmental delays or disorders. The role of the placenta in fetal brain development is unclear and is the focus of an emerging field known as neuroplacentology. In this review, we summarize neurodevelopmental outcomes in CHD and their brain imaging correlates both in utero and postnatally. We review differences in the structure and function of the placenta in pregnancies complicated by fetal CHD and introduce the concept of a placental inefficiency phenotype that occurs in severe forms of fetal CHD, characterized by a myriad of pathologies. We propose that in CHD placental dysfunction contributes to decreased fetal cerebral oxygen delivery resulting in poor brain growth, brain abnormalities, and impaired neurodevelopment. We conclude the review with key areas for future research in neuroplacentology in the fetal CHD population, including (1) differences in structure and function of the CHD placenta, (2) modifiable and nonmodifiable factors that impact the hemodynamic balance between placental and cerebral circulations, (3) interventions to improve placental function and protect brain development in utero, and (4) the role of genetic and epigenetic influences on the placenta–heart–brain connection. Impact Neuroplacentology seeks to understand placental connections to fetal brain development. In fetuses with CHD, brain growth abnormalities begin in utero. Placental microstructure as well as perfusion and function are abnormal in fetal CHD.

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