Fetal brain injury

Cerebral palsy is a salient example of fetal brain injury with many possible causes. I am not making an argument here that every case of cerebral palsy is a result of impacts on the fetal environment only that evidence suggests some cases may indeed have such a cause. Here are some facts10 ... 

Of all the likely prenatal factors in cerebral palsy, reduced blood flow to the fetal brain (cerebral ischemia) during gestation is the most important. The second most important is apparendy inflammation caused by intrauterine infection.12 Fetal inflammatory responses can evidendy contribute to brain injury by producing white matter lesions. In any case, inflammation resulting from infection of the chorio-amnion membrane system that surrounds the fetus (chorioamnionitis) is now a known causative factor for neurological disturbance and cerebral palsy. 

The recent confirmation that neurogenesis occurs in the adult brain, and isolation and characterization in vitro of neural progenitor and stem cells from the adult CNS, open new opportunities for cellular therapy in the CNS. Adult-derived neural progenitor and stem cells circumvent the ethical and political concerns associated with their embryonic and fetal counterparts, and offer the opportunity to treat a broad range of CNS diseases and injuries, making adult NSCs a model of choice for cellular therapy in the CNS. 

Cellular therapy is the replacement of lost or dysfunctional tissues with new ones. Various cell types have been evaluated and considered for therapy. In the CNS, fetal neuronal tissue has been particularly evaluated for its merit in treating neurological diseases and injuries [1]. While numerous experimental and clinical transplantation studies showed that fetal neuronal transplants improve functional deficits in models of CNS diseases [2-5], others reported less positive outcomes [6, 7]. In addition, the rate of survival of fetal neuronal cells transplanted into the adult brain is relatively low, requiring large quantities of tissue, generally from several fetuses, for therapy. Researchers are looking at other opportunities for cellular therapy, particularly in the CNS. 

The developing human brain is much more susceptible to injury caused by toxic agents than the brain of an adult. Probably all potential neurotoxic compounds would also cause damage to the developing brain and at much lower doses [1], Indeed, neuro-developmental disorders in children such as attention deficit, mental retardation or autism are often associated with the exposure to chemicals in the environment during early fetal and postnatal development [1-3]. 

The earliest of these developmental abnormalities involve the brain stem. In a unique case, Rodier et al. (1996) reported the nearly complete absence of the superior olive and facial nerve nucleus, with shortening of the brain stem between facial nerve nucleus and the trapezoid body. They concluded that the initiating injury in this autistic brain occurred around the time of neural tube closure, which occurs at about 4 weeks of fetal development (O Rahilly and Muller, 1994). This timing also corresponds to an increased incidence of autism following exposure to the drug thalidomide during pregnancy (Rodier and Hyman, 1998 Miller et al., 2005). 

While the amounts consumed rarely cause acute illness, these organophosphate insecticides (OPs) have the potential to cause long-term damage to the brain and the nervous system, which are rapidly growing and extremely vulnerable to injury during fetal development, infancy and early... 

Nickel carbonyl (nickel lelracarbonyl [CAS 13463-39-3]) inhalation of vapors can cause severe iung and systemic injury without irritantwarning signs. Symptoms include headache, nausea, vomiting, fever, and extreme weakness. Based on animal studies, liver and brain damage may occur. Adverse effects on fetal development in test animals. A carcinogen in test animals. 

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