Perinatal Hypoxic-Ischemic Encephalopathy

Abstract

Perinatal hypoxic-ischemic encephalopathy (HIE) is an important cause of brain injury in the newborn and can result in long-term devastating consequences. Perinatal hypoxia is a vital cause of long-term neurologic complications varying from mild behavioural deficits to severe seizure, mental retardation, and/or cerebral palsy in the newborn. In the mammalian developing brain, ongoing research into pathophysiological mechanism of neuronal injury and therapeutic strategy after perinatal hypoxia is still limited. With the advent of promising therapy of hypothermia in HIE, this paper reviews the pathophysiology of HIE and the future potential neuroprotective strategies for clinical potential for hypoxia sufferers.

Heme Oxygenase-1 Mediates Neuroprotection Conferred by Argon in Combination with Hypothermia in Neonatal Hypoxia–Ischemia Brain Injury

“…The protective effects are likely associated with intrinsic apoptotic and neuroinflammation pathway inhibition and cellular survival signal activation. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Introduction Hypoxic-ischaemic encephalopathy (HIE) is a major cause of mortality and disability in the newborn and is associated with cerebral palsy, epilepsy, mental retardation and learning difficulties 1 . HIE is associated with hugely negative emotion and financial costs to the family of the affected infant and the burden to society in general.…”

Preliminary case control study to establish the correlation between novel peroxidation biomarkers in cord serum and the severity of hypoxic ischemic encephalopathy

“…However, lactate production can be induced by non-hypoxic conditions such as glycogenolysis, alkalosis, or catecholamine infusion. Therefore, the reliability of the analysis of cord blood gases is of limited value in predicting HIE [5][6][7]. Moreover, the clinical methods employed to assess HIE which include Apgar score, amplitude integrated electroencephalography, and magnetic resonance imaging are useful for predicting some outcome of neonatal hypoxia but lack the sensitivity needed to implement effective therapies such as hypothermia [8].…”

Models of CNS injury in the nonhuman primate: A new era for treatment strategies

“…Although ablative injury is primarily observed following penetrating, ballistic or battlefield neurotrauma [34], this model bears more relevance to neurological deficits resulting as from the surgical resection of damaged cortical tissue, due to traumatic injury, tumours or masses [35] and surgical interventions for the treatment of epilepsy [36]. Surgically induced lesions of the orbital frontal cortex (OFC; Walker's area 11 and 13) and amygdala have also been preformed on the rhesus monkey (Macaca mulatta) using either aspiration or intracortical injections of neurotoxic compounds (ibotenic acid [37][38][39] [4]. A common sequelae of pHI is periventricular leukomalacia (PVL) which results in white matter lesions surrounding the periventricular region [45].…”

“…It is well established that the major pathological processes underlying HI injury is the deprivation of glucose and oxygen supplies, ultimately leading to necrotic cell death [49]. The subsequent reperfusion injury also exacerbates neurological damage by increasing oxidative stress and excitotoxicity [4]. Selective degeneration of interneurons in the NHP motor cortex has been demonstrated following perinatal HI insults [50].…”