Review

Wagner, Meredith; Ryu, Yun Kyoung; Smith, Sarah C.; Mintz, C. David

doi:10.1097/ana.0000000000000118

Cited by 37 publications

(11 citation statements)

References 65 publications

(67 reference statements)

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“…Recent studies investigating the effects of anesthesia on the developing brain suggest a risk of neurotoxicity. Even a few hours of exposure can result in significant neuronal loss in young animals, with deleterious effects persisting later in life (Brambrink et al., 2012; Creeley et al., 2013; Jevtovic-Todorovic et al., 2003; Wagner, Ryu, Smith, & Mintz, 2014). In children, the risk of learning disabilities increases with longer accumulated exposure to some drugs (Wilder et al., 2009).…”

Section: Introductionmentioning

confidence: 99%

The Parallel Auditory Brainstem Response

Polonenko

Maddox

2019

Trends in Hearing

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The frequency-specific tone-evoked auditory brainstem response (ABR) is an indispensable tool in both the audiology clinic and research laboratory. Most frequently, the toneburst ABR is used to estimate hearing thresholds in infants, toddlers, and other patients for whom behavioral testing is not feasible. Therefore, results of the ABR exam form the basis for decisions regarding interventions and hearing habilitation with implications extending far into the child’s future. Currently, responses are elicited by periodic sequences of toneburst stimuli presented serially to one ear at a time, which take a long time to measure multiple frequencies and intensities, and provide incomplete information if the infant wakes up early. Here, we describe a new method, the parallel ABR (pABR), which uses randomly timed toneburst stimuli to simultaneously acquire ABR waveforms to five frequencies in both ears. Here, we describe the pABR and quantify its effectiveness in addressing the greatest drawback of current methods: test duration. We show that in adults with normal hearing the pABR yields high-quality waveforms over a range of intensities, with similar morphology to the standard ABR in a fraction of the recording time. Furthermore, longer latencies and smaller amplitudes for low frequencies at a high intensity evoked by the pABR versus serial ABR suggest that responses may have better place specificity due to the masking provided by the other simultaneous toneburst sequences. Thus, the pABR has substantial potential for facilitating faster accumulation of more diagnostic information that is important for timely identification and treatment of hearing loss.

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Section: Introductionmentioning

confidence: 99%

The Parallel Auditory Brainstem Response

Polonenko

Maddox

2019

Trends in Hearing

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“…Numerous studies point to a variety of mechanisms by which anesthetics activate pro-apoptotic pathways, but it remains unclear whether apoptosis is a cause or consequence of PAN. In fact, it is probably not plausible to define a mechanism of PAN until the phenotype of the injury has become clear, and at present numerous competing hypotheses exist 115 . Future work on mechanisms of toxicity should be directed towards settling this question, extending currently identified putative mechanisms towards more advanced model systems, and to asking how existing mechanisms could be inter-related.…”

Section: Resultsmentioning

confidence: 99%

Molecular Mechanisms of Anesthetic Neurotoxicity: A Review of the Current Literature

Jackson

Gray

Jiang

et al. 2016

Journal of Neurosurgical Anesthesiology

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Data from epidemiologic studies and animal models have raised a concern that exposure to anesthetic agents during early postnatal life may cause lasting impairments in cognitive function. It is hypothesized that this is due to disruptions in brain development, but the mechanism underlying this toxic effect remains unknown. Ongoing research, particularly in rodents, has begun to address this question. In this review we examine currently postulated molecular mechanisms of anesthetic toxicity in the developing brain, including effects on cell death pathways, growth factor signaling systems, NMDA and GABA receptors, mitochondria, and epigenetic factors. The level of evidence for each putative mechanism is critically evaluated, and we attempt to draw connections between them where it is possible to do so. While there are many promising avenues of research, at this time no consensus can be reached as to a definitive mechanism of injury.

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“…48 Additional studies to characterize the morphology and physiology of exposed granule cells will be needed to determine whether they function normally. 49 …”

Section: Discussionmentioning

confidence: 99%

Long-term Fate Mapping to Assess the Impact of Postnatal Isoflurane Exposure on Hippocampal Progenitor Cell Productivity

et al. 2016

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Background Exposure to isoflurane increases apoptosis among postnatally generated hippocampal dentate granule cells. These neurons play important roles in cognition and behavior, so their permanent loss could explain deficits after surgical procedures. Methods To determine whether developmental anesthesia exposure leads to persistent deficits in granule cell numbers, a genetic fate-mapping approach to label a cohort of postnatally generated granule cells in Gli1-CreERT2::GFP bitransgenic mice was utilized. Green fluorescent protein (GFP) expression was induced on postnatal day 7 (P7) to fate map progenitor cells, and mice were exposed to 6 h of 1.5% isoflurane or room air 2 weeks later (P21). Brain structure was assessed immediately after anesthesia exposure (n = 7 controls and 8 anesthesia-treated mice) or after a 60-day recovery (n = 8 controls and 8 anesthesia-treated mice). A final group of C57BL/6 mice was exposed to isoflurane at P21 and examined using neurogenesis and cell death markers after a 14-day recovery (n = 10 controls and 16 anesthesia-treated mice). Results Isoflurane significantly increased apoptosis immediately after exposure, leading to cell death among 11% of GFP-labeled cells. Sixty days after isoflurane exposure, the number of GFP-expressing granule cells in treated animals was indistinguishable from control animals. Rates of neurogenesis were equivalent among groups at both 2 weeks and 2 months after treatment. Conclusions These findings suggest that the dentate gyrus can restore normal neuron numbers after a single, developmental exposure to isoflurane. The authors’ results do not preclude the possibility that the affected population may exhibit more subtle structural or functional deficits. Nonetheless, the dentate appears to exhibit greater resiliency relative to nonneurogenic brain regions, which exhibit permanent neuron loss after isoflurane exposure.

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Review

Cited by 37 publications

References 65 publications

The Parallel Auditory Brainstem Response

The Parallel Auditory Brainstem Response

Molecular Mechanisms of Anesthetic Neurotoxicity: A Review of the Current Literature

Long-term Fate Mapping to Assess the Impact of Postnatal Isoflurane Exposure on Hippocampal Progenitor Cell Productivity

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