Anesthesiology and Clinical Science Research

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (202) 780-3397

Commentary - Anesthesiology and Clinical Science Research (2025) Volume 9, Issue 1

Anesthesia-induced neurotoxicity: Investigating long-term impacts on cognitive function

Sarah Thompson *

Department of Neuroanesthesia, University of Berlin, Germany

*Corresponding Author:
Sarah Thompson
Department of Neuroanesthesia, University of Berlin, Germany
E-mail: thmpsara@qq.de

Received: 03-Mar-2025, Manuscript No. AAACSR-25-162690; Editor assigned: 04-Mar-2025, PreQC No. AAACSR-25-162690; Reviewed:18-Mar-2025, QC No. AAACSR-25-162690; Revised:24-Mar-2025, Manuscript No. AAACSR-25-162690(R); Published:31-Mar-2025, DOI:10.35841/ aaacsr-9.1.207

Citation: Thompson S. Anesthesia-induced neurotoxicity: Investigating long-term impacts on cognitive function. Anaesthesiol Clin Sci Res 2025;9(1):207

Visit for more related articles at Anesthesiology and Clinical Science Research

Introduction

Anesthesia is a critical component of modern surgery, allowing patients to undergo procedures with minimal pain and discomfort. However, growing concerns have emerged regarding the long-term effects of anesthetic agents, particularly in vulnerable populations, and their potential to induce neurotoxicity in the brain. Anesthesia-induced neurotoxicity (AIN) refers to the damaging effects that anesthetic agents may have on the brain, leading to alterations in cognitive function that may persist long after the effects of the anesthetics themselves have worn off. While the primary purpose of anesthesia is to induce a temporary state of unconsciousness, research has increasingly focused on how anesthetic exposure can lead to long-term cognitive impairments, especially in older adults and young children. This article explores the mechanisms behind anesthesia-induced neurotoxicity, its potential long-term effects on cognitive function, and the factors influencing its occurrence [1].

The mechanisms underlying anesthesia-induced neurotoxicity are complex and still not fully understood, but research suggests that they involve the disruption of neural circuits and cellular structures within the brain. One of the primary mechanisms believed to be at play is neuroinflammation, a process in which the immune system becomes activated in response to injury or stress in the brain. Many anesthetic agents, including volatile anesthetics like sevoflurane and isoflurane, as well as intravenous agents like propofol, have been shown to activate glial cells, which are involved in inflammatory responses in the central nervous system. These inflammatory processes can lead to neuronal damage, apoptosis (programmed cell death), and changes in synaptic plasticity, all of which may contribute to cognitive dysfunction [2].

In addition to neuroinflammation, another critical factor involved in anesthesia-induced neurotoxicity is the disruption of synaptic development and neuroplasticity. In both pediatric and adult populations, exposure to anesthetics has been associated with changes in the brain's ability to form new neural connections. Studies in animals, particularly in neonates and young animals, have demonstrated that exposure to certain anesthetic agents can lead to neuronal cell death and a reduction in synaptic connections, particularly in regions of the brain responsible for learning, memory, and higher cognitive functions, such as the hippocampus and prefrontal cortex. These findings have led to concerns about the potential long-term impact of anesthesia on cognitive function, particularly in children who are undergoing surgical procedures during critical periods of brain development [3, 4].

In pediatric patients, there is mounting evidence to suggest that early exposure to anesthetic agents may lead to long-term cognitive deficits, including impairments in learning, memory, and attention. Animal studies have shown that anesthesia exposure during early brain development can result in significant changes to brain architecture, and some studies in humans have raised similar concerns. For example, children who have undergone multiple surgeries requiring general anesthesia before the age of three have been reported to exhibit developmental delays and cognitive deficits later in life. While the evidence in human studies is still inconclusive, there is enough concern to warrant further investigation into the potential risks of anesthesia exposure in early childhood. Given the rapid and significant brain development that occurs in the early years of life, the potential for long-lasting neurotoxic effects is an area of ongoing research [4, 5, 6].

In older adults, anesthesia-induced neurotoxicity manifests primarily as postoperative cognitive dysfunction (POCD). POCD is characterized by a decline in cognitive abilities, including memory loss, difficulty concentrating, and problems with executive function, which typically presents after surgery and can last for weeks or even months. While POCD can occur in patients of any age, older adults are particularly vulnerable, with studies showing that up to 25% of elderly patients may experience some degree of cognitive decline after surgery. The risk factors for POCD include advanced age, pre-existing cognitive impairment, and the complexity of the surgical procedure. Although the exact pathophysiology of POCD is not fully understood, it is thought to be related to the inflammatory response triggered by anesthesia, as well as alterations in brain connectivity and neuroplasticity. The combination of anesthesia and surgery may exacerbate underlying neurodegenerative conditions such as Alzheimer’s disease, making older patients more susceptible to cognitive decline [7, 8].

Despite the growing body of research on anesthesia-induced neurotoxicity, there is still much to learn about the long-term effects of anesthetics on the brain. Several factors influence an individual’s risk of developing neurotoxicity, including the type of anesthesia used, the age of the patient, the duration of exposure, and the presence of underlying health conditions. For instance, the use of volatile anesthetics like sevoflurane and isoflurane has been linked to greater neurotoxic effects compared to intravenous agents like propofol, particularly when used for prolonged periods. Additionally, children who undergo multiple surgeries or who are exposed to anesthesia at a very young age may face a higher risk of neurodevelopmental delays, as the brain is in a critical stage of maturation. Similarly, older adults with pre-existing cognitive decline or those undergoing complex surgeries may have an increased susceptibility to the cognitive effects of anesthesia [9].

To mitigate the potential neurotoxic effects of anesthesia, clinicians are increasingly turning to strategies such as depth-of-anesthesia monitoring, neuroprotective agents, and minimizing anesthesia exposure in high-risk populations. Depth-of-anesthesia monitoring, which involves assessing brain activity during surgery, can help prevent the administration of excessive amounts of anesthetic agents, potentially reducing the risk of neurotoxicity. Furthermore, researchers are investigating neuroprotective drugs that could counteract the harmful effects of anesthesia on the brain. For example, agents that block the inflammatory response or promote neuronal survival and repair are being explored as potential treatments to minimize anesthesia-induced brain damage [10].

Conclusion

Anesthesia-induced neurotoxicity is a growing concern, particularly regarding its long-term effects on cognitive function in vulnerable populations such as young children and older adults. While much progress has been made in understanding the mechanisms of neurotoxicity, further research is needed to determine the full extent of the risks associated with anesthetic exposure and to develop strategies to prevent or mitigate these effects. By improving our understanding of how anesthetics affect the brain, healthcare providers can make more informed decisions about the safest approaches to anesthesia, ultimately improving patient outcomes and minimizing the potential for cognitive impairments in the future. As the field of anesthesia and neuroscience continues to evolve, the focus on patient safety and brain health will remain paramount in ensuring that the benefits of anesthesia outweigh the risks for all patients.

References

  1. Imura H, Caputo M, Parry A, et al. Age-dependent and hypoxia-related differences in myocardial protection during pediatric open heart surgery. Circ. 2001;103(11):1551-6.
  2. Indexed atGoogle ScholarCross Ref

  3. Immer FF, Stocker F, Seiler AM, et al. Troponin-I for prediction of early postoperative course after pediatric cardiac surgery. J Am Coll Cardiol. 1999;33(6):1719-23.
  4. Indexed atGoogle ScholarCross Ref

  5. Gupta-Malhotra M, Kern JH, Flynn PA, et al. Cardiac troponin I after cardiopulmonary bypass in infants in comparison with older children. Cardiol Young. 2013;23(3):431-5.
  6. Indexed atGoogle ScholarCross Ref

  7. Landoni G, Biondi-Zoccai GG, Zangrillo A, et al. Desflurane and sevoflurane in cardiac surgery: A meta-analysis of randomized clinical trials. J Cardiothorac Vasc Anesth.;21(4):502-11.
  8. Indexed atGoogle ScholarCross Ref

  9. De Hert SG, Van der Linden PJ, Cromheecke S, et al. Cardioprotective properties of sevoflurane in patients undergoing coronary surgery with cardiopulmonary bypass are related to the modalities of its administration. The Journal of the American Society of Anesthesiologists. 2004;101(2):299-310.
  10. Indexed atGoogle ScholarCross Ref

  11. Piriou V, Mantz J, Goldfarb G, et al. Sevoflurane preconditioning at 1 MAC only provides limited protection in patients undergoing coronary artery bypass surgery: a randomized bi-centre trial. Br J Anaesth. 2007;99(5):624-31.
  12. Indexed atGoogle ScholarCross Ref

  13. Bettex DA, Wanner PM, Bosshart M, et al. Role of sevoflurane in organ protection during cardiac surgery in children: a randomized controlled trial. Interact Cardiovasc Thorac Surg. 2015;20(2):157-65.
  14. Indexed atGoogle ScholarCross Ref

  15. Mishra J, Dent C, Tarabishi R, et al. Neutrophil gelatinase-associated lipocalin (NGAL) as a biomarker for acute renal injury after cardiac surgery. Lancet. 2005;365(9466):1231-8.
  16. Indexed atGoogle ScholarCross Ref

  17. Friedrich MG, Bougioukas I, Kolle J, et al. NGAL expression during cardiopulmonary bypass does not predict severity of postoperative acute kidney injury. BMC Nephrol. 2017;18(1):1-7.
  18. Indexed atGoogle ScholarCross Ref

  19. Owens GE, King K, Gurney JG, et al. Low renal oximetry correlates with acute kidney injury after infant cardiac surgery. Pediatr Cardiol. 2011;32:183-8.

Indexed atGoogle ScholarCross Ref

 

 

Get the App