Introduction
Perinatal brain damage is a collective term that describes the effects of an injury on the baby's developing brain. The primary causes are frequently listed as periventricular leukomalacia (brain injury in premature babies), intraventricular hemorrhage (bleeding in the brain), hypoxic-ischemic encephalopathy (brain injury due to lack of oxygen), and neonatal stroke (stroke in newborns). Cerebral palsy (a group of conditions affecting movement) and encephalopathy of prematurity (brain injury in premature infants) are occasionally included as causes of perinatal brain damage, although they describe clinical syndromes or symptoms that may (or may not) be caused by perinatal brain damage.
What Is Perinatal Brain Damage?
Perinatal brain damage occurs often in both developed and developing countries. Seizures and decreased responsiveness are the most common clinical signs of newborn encephalopathy (a group of conditions that results in brain dysfunction), which is caused by almost all types of prenatal brain injury. While birth trauma injuries generally occur more frequently in full-term neonates, perinatal brain damage encompasses all brain injuries that take place during the perinatal period (begins from 20 to 28th weeks of gestation and ends 1 to 4 weeks after delivery) in newborns of all gestational ages. Birth trauma has become less common as a result of significant advancements in prenatal care.
What Is the Pathophysiology of Perinatal Brain Damage?
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Severe intrauterine hypoxia (oxygen deficiency) is the primary cause of acute hypoxic-ischemic brain damage in neonates, with a few exceptions. Usually, an abrupt decrease in the uterine or umbilical circulation causes this, which can also result from abruption placenta (placental separation), uterine contracture, umbilical cord compression, etc.
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There are various stages in the development of brain damage. When cerebral hypoxia is severe enough to exhaust tissue energy stores (primary phase), it is frequently followed by nearly full recovery of glucose consumption, mitochondrial respiration, and the production of high-energy phosphates following reperfusion (restoration of blood flow)and reoxygenation (latent phase).
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Subsequently, a subsequent phase, also known as secondary brain injury or secondary energy failure occurs, involving a drop in high-energy phosphates and cell death. The mechanisms underlying long-term cell injury and healing (tertiary phase) are poorly understood, and current therapy approaches have primarily addressed the latent period.
What Are the Common Conditions That Occur Due to Perinatal Brain Damage?
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Perinatal Asphyxia: The term "perinatal asphyxia," sometimes known as "birth asphyxia," refers to a situation in which there is insufficient blood flow or defective gas exchange, resulting in hypoxemia (low oxygen in the blood) and hypercapnia (elevated levels of carbon dioxide in the blood), and that develops concurrently with labor and delivery. While, multi-organ dysfunction is prevalent and can affect all organs, particularly the respiratory and cardiovascular tract.
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Hypoxic-Ischemic Encephalopathy: The non-specific name for brain dysfunction brought on by insufficient oxygen and blood flow to the brain is hypoxic-ischemic encephalopathy (HIE). The prevalence of HIE varies greatly throughout the world. In wealthy countries, 1 out of every 1,000 live births is affected by HIE, while it is far more common in developing nations. Generally, one-third of neonates with severe illness pass away, and between 30 and 40 percent of those who survive experience deficits such as cerebral palsy, seizures, and problems with motor, cognitive, and memory. For full-term infants, mild neonatal encephalopathy has an excellent prognosis and a high likelihood of normal follow-up.
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Cerebral Palsy: Cerebral palsy is a clinical condition that results from a non-progressive brain lesion in a fetus or child, resulting in permanent disability. Muscle tone, reflexes, equilibrium, balance, coordination, and control over movement are all impacted by cerebral palsy. Moreover, it may affect oral motor functions and gross, and fine motor skills.
The cause of cerebral palsy (CP) is complicated, multifactorial, and challenging to determine in a single child. Although hypoxic-ischemic encephalopathy in full-term infants has also been somewhat linked to cerebral palsy, CP primarily affects preterm infants. The prevalence of cerebral palsy varies amongst the populations under study, ranging from less than 10 % to more than 30 %, in newborns with and without an acute hypoxic episode at birth.
What Are the Risk Factors for Perinatal Brain Damage?
Based on studies, three main categories of risk factors have been established and identified for perinatal encephalopathy. They are infection or inflammation (e.g., chorioamnionitis), chronic mal perfusion or hypoxia (e.g., fetal growth restriction), and premature delivery or prematurity. Maternal socioeconomic position and health history, a family history of neurologic disease, and the influence of genetics and epigenetics are factors that are frequently overlooked. It appears that maternal obesity is an additional risk factor on its own. Even after controlling for delivery mode and maternal risk variables, newborns of obese mothers were confirmed with perinatal brain injuries more frequently than infants of non-obese mothers.
How Perinatal Brain Damage Is Managed?
Therapeutic hypothermia is presently the only available treatment that has been shown to enhance neurologic long-term outcomes in full-term and premature infants with HIE. The primary method of treatment for neonatal hypoxic-ischaemic damage in term infants is therapeutic hypothermia employing a targeted temperature-lowering regimen consisting of sequential periods of moderate chilling, maintenance, and delayed rewarming.
Cooling lowers brain metabolism, which in turn lowers the phase of secondary energy failure that occurs after an acute hypoxic-ischemic shock. There is little information available on treating patients later on. Cooling should be initiated within 6 hours to be neuroprotective. Therapeutic hypothermia reduces cerebral palsy, increases survival, and enhances neurodevelopmental outcomes at 18 months. Other possible treatment options, which target oxidative stress and inflammation after the initial injury, are either not currently in clinical trials or have not shown any signs of efficacy.
Conclusion
The causes and contributing factors of perinatal brain injury are typically complex, and a complete understanding of them is still relatively incomplete. Acute hypoxic episodes during delivery may play a less significant influence on perinatal brain damage, particularly in situations where intrauterine inflammation, preterm, persistent hypoxia or growth retardation, and genetic abnormalities seem to be more major contributors. A significant issue in the medical field is still accurately identifying the fetus "at risk" for a neurologic outcome at any gestational age.
