Journal of Neonatal Biology

The Role of Neonatal Stroke in Human Brain

Stephen Ashwal Department of Radiology and Imaging Sciences, Emory University and Children’s Healthcare of Atlanta, Atlanta, GA, USA

Received: 01-Jun-2022, Manuscript No. JNB-22-17441; Editor assigned: 06-Jun-2022, Pre QC No. JNB-22-17441(PQ); Reviewed: 22-Jun-2022, QC No. JNB-22-17441; Revised: 27-Jun-2022, Manuscript No. JNB-22-17441(R); Published: 04-Jul-2022, DOI: 10.35248/2167-0897.22.11.352

Description

Common perinatal arterial ischemic stroke causes serious longterm neurologic and cognitive abnormalities, including cerebral palsy, epilepsy, neurodevelopmental disabilities, behavioral problems, and poor visual and language function. It also causes major morbidity. The majority of cerebral palsy cases have a cerebrovascular localized or global insult as their etiology, and more than half of all children with the condition are born at term. Perinatal brain injury has been shown to have a complex etiology. Over the past two decades, much has been learned about how the stroke phenotype differs in different age groups compared to adults, as well as the underlying causes and pathophysiology thanks to the accessibility and safe use of Magnetic Resonance Imaging (MRI) in newborns, older babies, and children. There are typically two ways that perinatal stroke manifests.

Early on in a child's life, signs may be noticed. The most common symptom of prenatal stroke is seizures. A baby could, however, also be lethargic or have respiratory issues. This is a possible presentation for AIS, CSVT, and HS in newborns. An "acute symptomatic neonatal stroke" is what this is. The majority of neonates do not exhibit an abrupt onset of symptoms, unlike older children and adults. Symptoms could be noticed later in childhood. Stroke can sometimes happen before birth or without causing convulsions. Early hand preference or similar asymmetry in motor development may be the earliest symptom of stroke in these situations. These symptoms commonly appear in parents' infants around the age of 6 months.

The effects of localized damage on the mature brain are complex but are becoming more understood. Neurodevelopmental factors add to the complexity of the developing brain. This subject is eloquently covered elsewhere, but is succinctly outlined here to serve as a framework for the discussion of results that follows. The timing of acquired brain injuries, such as strokes, during pregnancy adds a number of frequently conflicting circumstances that will ultimately influence the result in terms of brain maturation and development. These include synaptogenesis, myelination, pruning, and neuronal maturation and structure. After general or focused ischemia-reperfusion, neuronal apoptosis is frequently seen, can be fairly severe, and decreases with maturity. Due in part to the high expression of many essential elements of apoptotic pathways that prevent neuronal overproduction during early brain development, apoptotic pathways are more easily activated in the developing brain (programmed neuronal death).

Although apoptosis and autophagy have traditionally been associated with delayed cell death in the ischemic penumbra and necrosis with early neuronal death in the ischemic core, apoptosis is an essential contributing neuronal death mechanism in the core following new localized stroke. Neonatal encephalopathies, which resemble perinatal strokes, can be observed in conjunction with periventricular and intraventricular haemorrhage, diffuse cerebral injury following global cerebral hypoxic-ischemic insults, and periventricular leukomalacia, which is commonly found in preterm newborns. There is definitely hope for a good life after a prenatal stroke. Many children have good levels of functioning despite having significant brain lesions, which is a fascinating illustration of the potential power of developmental plasticity. It frequently causes impairments like cerebral palsy. Brain imaging is necessary for the diagnosis of this illness.