The Etiology and Evolution of Fetal Brain Injury

نویسنده

  • Andrew Macnab
چکیده

The nine months of intrauterine life are a continuum during which a series of situations and events can occur that result in abnormalities of normal brain growth or injury to the developing brain of the fetus. Genetic mutations and hereditary syndromes can predispose the fetus to intrauterine death, mortality in early life, and various degrees and combinations of brain injury and neurological deficits. Structural brain injury occurs due to a number of well defined and some relatively obscure causes. Premature delivery puts the fetus at risk of complications during birth and in the early days of life that can compromise the brain. Such infants have systems that are physiologically too immature to function normally, making them dependent on a range of care entities many of which are known to have risks associated with their use. The end result especially when prematurity is of extreme degree, is a significant incidence of cognitive and motor deficits. Maternal infection is increasingly recognized to precipitate premature labour and produce inflammatory by-products that cross the placenta and increase the vulnerability of the fetus to brain injury. (Gotsch et al, 2007; Kendall & Peebles 2005; Mercer 2004) Various pathologies related to the placenta also compromise the well being of the fetus. Impaired fetal growth secondary to placental insufficiency is associated with a reduction in the number of brain cells formed by the time the infant is born; growth retarded infants are at increased risk of hypoxic stress and hypoxic ischemic brain injury due to failure of placental blood flow, gas exchange and fetal oxygen delivery. Suboptimal nutrition also poses the risk of hypoglycaemic brain injury immediately after birth. Post mature infants are at risk from placental failure, hypoxic ischaemic injury and birth trauma. Infants conceived with in-vitro fertilization are at increased risk of neurological disability, especially cerebral palsy. (Stromberg et al 2002) Stroke is a significant cause of neurodevelopmental morbidity in newborn infants that can result in permanent sequelae and may be underreported. (Ozduman et al 2004) The overall incidence of cerebral palsy has not been reduced significantly in spite of advances in obstetric care, and CP remains a significant cause for motor deficits and cognitive disability that become evident in early life and result in permanent disability.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

P 104: Effects of Human Neural Stem Cells in Cure Neuroinflammation of Traumatic Brain Injury

Traumatic brain injury (TBI) is defined as an external mechanical injury to the brain. Neuroinflammation plays a vital role in the pathophysiology of TBI. Microglia and astrocytes play a central role in the initiation and regulation of inflammation. Numerous pro-inflammatory mediators including cytokines, chemokines, reactive oxygen species (ROS) and nitric oxide (NO) released by microglia. In ...

متن کامل

The impact of COVID-19 during pregnancy on fetal brain development

The development of the brain as the most complex structure of the human body is a long process that begins in the third week of pregnancy and continues until adulthood and even until the end of life (1). Human brain myelination begins one to two months before birth in the visual system and eventually lasts until the age of two in other sensory systems and then the motor systems (4). Processes a...

متن کامل

Social life, evolution of intelligence, behaviour and human brain size

Social life is one of the most critical factors of the evolution of the behavior of non-human primates and humans. Several factors, such as an increase in brain size, adaptive modules, and grooming, are related to the complexities of social groups. Although some scientists have mentioned foraging as a rival hypothesis for the evolution of behavior, in this research, we tried to investigate the ...

متن کامل

The Effects of Estrogen Receptors' Antagonist on Brain Edema, Intracranial Pressure and Neurological Outcomes after Traumatic Brain Injury in Rat

Background: In previous studies, the neuroprotective effect of 17&beta-estradiol in diffuse traumatic brain injury has been shown. This study used ICI 182,780, a non-selective estrogen receptor antagonist, to test the hypothesis that the neuroprotective effect of 17&beta-estradiol in traumatic brain injury is mediated by the estrogen receptors. Methods: The ovariectomized rats were divided into...

متن کامل

P80: The Effects of Progesterone Receptors\' Antagonist RU-486 on BrainEdema, Intracranial Pressure and Neurological Outcomes after Traumatic Brain Injury

In previous studies, the neuroprotective effect of progestrone in diffuse traumatic brain injury has been shown. This study used mifepristone (RU-486), a potent progesterone receptor antagonist, to evaluatethe hypothesis that the neuroprotective effect of progesterone in traumatic brain injury is mediated by the progesterone receptors. The ovariectomized rats were divided into 6 groups. Brain i...

متن کامل

Comparison the Accuracy of Fetal Brain Extraction from T2-Half-Fourier Acquisition Single-Shot Turbo Spin-Echo (HASTE) MR Image with T2-True Fast Imaging with Steady State Free Precession (TRUFI) MR Image by Level Set Algorithm

Background Access to appropriate images of fetal brain can greatly assist to diagnose of probable abnormalities. The aim of this study was to compare the suitability of T2-True Fast Imaging with Steady State Free Precession (T2-TRUFI), and T2-Half-Fourier Acquisition Single-Shot Turbo Spin-Echo (T2- HASTE( magnetic resonance imaging (MRI) to extract the fetal brain using the level set algorithm...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2012