Perinatal Hypoxic Ischemic Encephalopathy (HIE) is a major cause of neonatal mortality and irreversible damage to the brain, leading to a variety of neurodevelopmental long-term disabilities. Nowadays tools for accurate early diagnosis and prediction of long-term outcome are still lacking particularly for neonates with mild-to-moderate HIE based on early magnetic resonance imaging and electroencephalography (EEG) findings [1]. Integrated clinical neurophysiology, where the EEG is combined with multimodal evoked potentials (EPs) can assist the neurological prognosis of newborn infants with HIE, by early identification of the extent of brain dysfunction and the potential for recovery, at bedside [2]. This important topic of research, is not yet fully explored and the use of multimodal neurophysiological tools has not yet entered the clinical practice. In this issue of the European Journal of Paediatric Neurology, Delval et al. [3] report a cohort of neonates undergoing therapeutic hypothermia (TH) for HIE who had multimodal EPs (both SEP and BAEP) at the withdrawal of TH, associated with continuous EEG. They used a standardized classification model for grading the severity of both neurophysiological and outcome measures and found that adding multimodal evoked potentials to demographic, clinical and EEG data allowed to correctly classify the outcome at one and two years in all 30 neonates recorded. EPs explore the functioning of the sensory pathways afferent to the cortex. Changes in latency, amplitude and morphology of the responses can be quantified and compared with normal responses for age, giving functional information on brain regions susceptible to asphyxia, with prognostic value even in the absence of abnormalities on neuroimaging [4]. The main issue for the use of evoked potentials in neonates is reliability. Delval et al. [3] summarize in the discussion useful tips to improve the reliability and prognostic yield of these tests. Moreover, an integrated neurophysiological approach with somatosensory evoked potentials recorded at bedside in neonatal intensive care units, during EEG monitoring, has been recently proposed and implemented with normative values, demonstrating that it is a feasible, reliable and safe procedure [5]. Despite the study population is not large, the study by Delval et al. [3] confirms the ever-increasing literature data on the important prognostic role of evoked potentials in perinatal HIE and the importance of an integrated neurophysiological approach. Noteworthy, an improvement of EEG following TH, was a criterion for a better outcome, highlighting the importance of repeating the EEG after rewarming. By contrast, the combination of abnormal evoked potentials with failure to improve of the EEG proved to be an excellent predictor of severe prognosis. Thus, as the authors suggested, EEG and EPs should be systematically recorded following rewarming, to improve the prognostic assessment of perinatal hypoxic-ischemic encephalopathy

The added value of multimodal neurophysiological tools in the prognostic assessment of perinatal hypoxic-ischemic encephalopathy

Suppiej A.
2022

Abstract

Perinatal Hypoxic Ischemic Encephalopathy (HIE) is a major cause of neonatal mortality and irreversible damage to the brain, leading to a variety of neurodevelopmental long-term disabilities. Nowadays tools for accurate early diagnosis and prediction of long-term outcome are still lacking particularly for neonates with mild-to-moderate HIE based on early magnetic resonance imaging and electroencephalography (EEG) findings [1]. Integrated clinical neurophysiology, where the EEG is combined with multimodal evoked potentials (EPs) can assist the neurological prognosis of newborn infants with HIE, by early identification of the extent of brain dysfunction and the potential for recovery, at bedside [2]. This important topic of research, is not yet fully explored and the use of multimodal neurophysiological tools has not yet entered the clinical practice. In this issue of the European Journal of Paediatric Neurology, Delval et al. [3] report a cohort of neonates undergoing therapeutic hypothermia (TH) for HIE who had multimodal EPs (both SEP and BAEP) at the withdrawal of TH, associated with continuous EEG. They used a standardized classification model for grading the severity of both neurophysiological and outcome measures and found that adding multimodal evoked potentials to demographic, clinical and EEG data allowed to correctly classify the outcome at one and two years in all 30 neonates recorded. EPs explore the functioning of the sensory pathways afferent to the cortex. Changes in latency, amplitude and morphology of the responses can be quantified and compared with normal responses for age, giving functional information on brain regions susceptible to asphyxia, with prognostic value even in the absence of abnormalities on neuroimaging [4]. The main issue for the use of evoked potentials in neonates is reliability. Delval et al. [3] summarize in the discussion useful tips to improve the reliability and prognostic yield of these tests. Moreover, an integrated neurophysiological approach with somatosensory evoked potentials recorded at bedside in neonatal intensive care units, during EEG monitoring, has been recently proposed and implemented with normative values, demonstrating that it is a feasible, reliable and safe procedure [5]. Despite the study population is not large, the study by Delval et al. [3] confirms the ever-increasing literature data on the important prognostic role of evoked potentials in perinatal HIE and the importance of an integrated neurophysiological approach. Noteworthy, an improvement of EEG following TH, was a criterion for a better outcome, highlighting the importance of repeating the EEG after rewarming. By contrast, the combination of abnormal evoked potentials with failure to improve of the EEG proved to be an excellent predictor of severe prognosis. Thus, as the authors suggested, EEG and EPs should be systematically recorded following rewarming, to improve the prognostic assessment of perinatal hypoxic-ischemic encephalopathy
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/2475625
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