Latent Phase Identification of High-Frequency Micro-Scale Gamma Spike Transients in the Hypoxic Ischemic EEG of Preterm Fetal Sheep Using Spectral Analysis and Fuzzy Classifiers.

Hamid Abbasi,Laura Bennet,Alistair J Gunn,Charles P Unsworth

doi:10.3390/s20051424

Abstract

Premature babies are at high risk of serious neurodevelopmental disabilities, which in many cases are related to perinatal hypoxic–ischemic encephalopathy (HIE). Studies of neuroprotection in animal models consistently suggest that treatment must be started as early as possible in the first 6 h after hypoxia–ischemia (HI), the so-called latent phase before secondary deterioration, to improve outcomes. We have shown in preterm sheep that EEG biomarkers of injury, in the form of high-frequency micro-scale spike transients, develop and evolve in this critical latent phase after severe asphyxia. Real-time automatic identification of such events is important for the early and accurate detection of HI injury, so that the right treatment can be implemented at the right time. We have previously reported successful strategies for accurate identification of EEG patterns after HI. In this study, we report an alternative high-performance approach based on the fusion of spectral Fourier analysis and Type-I fuzzy classifiers (FFT-Type-I-FLC). We assessed its performance in over 2520 min of latent phase EEG recordings from seven asphyxiated in utero preterm fetal sheep exposed to a range of different occlusion periods. The FFT-Type-I-FLC classifier demonstrated 98.9 ± 1.0% accuracy for identification of high-frequency spike transients in the gamma frequency band (namely 80–120 Hz) post-HI. The spectral-based approach (FFT-Type-I-FLC classifier) has similar accuracy to our previous reverse biorthogonal wavelets rbio2.8 basis function and type-1 fuzzy classifier (rbio-WT-Type-1-FLC), providing competitive performance (within the margin of error: 0.89%), but it is computationally simpler and would be readily adapted to identify other potentially relevant EEG waveforms.

Highlights

Newborns with signs of hypoxic–ischemic encephalopathy (HIE) are critically at risk of developing lifelong debilitating conditions such as cognitive disorders, epilepsy, and cerebral palsy [1,2,3]
We assessed its performance in over min of latent phase EEG recordings from seven asphyxiated in utero preterm fetal sheep exposed to a range of different occlusion periods
Sensors 2020, 20, 1424 end of the latent phase causes subcortical neural cells to die over hours to days during a secondary phase lasting 48–72 h [4,5,6,7,8,9]

Summary

Introduction

Newborns with signs of hypoxic–ischemic encephalopathy (HIE) are critically at risk of developing lifelong debilitating conditions such as cognitive disorders, epilepsy, and cerebral palsy [1,2,3]. An. HI event, is associated with profound suppression of EEG activity. After the period of HI, EEG activity progressively recovers along with restoration of cerebral metabolism, during a latent phase of recovery for approximately 6 h [4,5,6,7,8]. The progressive failure of oxidative metabolism from the Sensors 2020, 20, 1424; doi:10.3390/s20051424 www.mdpi.com/journal/sensors. Sensors 2020, 20, 1424 end of the latent phase causes subcortical neural cells to die over hours to days during a secondary phase lasting 48–72 h [4,5,6,7,8,9]. The secondary phase is characterized by the appearance of high-amplitude stereotypic evolving seizures in the EEG recordings. The pioneers in our team, Gunn and Bennet, have demonstrated that the latent phase is the key time period that provides the optimal opportunity to initiate neuroprotective treatment before it is too late [2,7,11,12]

Methods

Results

Conclusion