Discover the causes and effects of memory loss after general anesthesia. Detailed advice and explanations to understand this phenomenon. Click to learn more. General anesthesia regularly raises questions, particularly concerning potential memory loss after the procedure. This phenomenon, called postoperative cognitive impairment, can affect cognitive faculties such as memory and concentration. Although these disorders are often transient, their intensity and duration can vary depending on several factors. Postoperative cognitive disorders are included in a broader term of postoperative neurocognitive disorders (PNDs), which also include postoperative delirium, an acute state of confusion and inattention, and postoperative cognitive dysfunction (POCD), a prolonged state of cognitive impairment primarily affecting high-level cognitive functions and memory. Recent data suggest an underlying relationship between delirium and POCD in patients whose brains may be vulnerable to cognitive decline after the stress of surgery and anesthesia.

It is essential to understand the mechanisms and risk factors associated with these effects. Studies have shown that certain factors, such as advanced age or specific medical history, may increase the likelihood of postoperative cognitive impairment. However, these impacts are generally mild and temporary. Risk factors for postoperative cognitive disorders include age, sepsis, cerebral vulnerability, frailty syndrome, complex and major surgeries (thoracic or cardiac), and repeated anesthetics. Patient frailty is based on physical performance, walking speed, daily physical activity, nutritional status, mental health, and cognition.

To minimize these risks, various medical and monitoring protocols are available to better support patients after anesthesia. Clear information and tailored advice help reduce anxiety and improve the management of potential side effects.

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What is general anesthesia?

General anesthesia (GA) is a temporary medical state, induced in a controlled manner, to suspend consciousness and painful perception. This method allows to perform both complex surgical interventions and certain invasive examinations in optimal conditions, without pain or memory of the surgical procedure.

Different types of anesthetics used

General anesthesia is based on the combination of several complementary drugs, each contributing precisely to the desired effect. The main agents used include:

• Hypnotics, such as propofol, etomidate, ketamine, or thiopental, administered intravenously, inducing a state of artificial sleep allowing the patient to be "put to sleep". Propofol, etomidate, and thiopental can produce a burst suppression electroencephalogram (EEG) at high doses.
• Analgesics, including sufentanil, fentanyl, remifentanil, and alfentanil, which act to effectively suppress pain during the procedure.
• Muscle relaxants, such as cisatracurium, atracurium, rocuronium, suxamethonium, and mivacurium, which reduce muscle tone by promoting a state of complete relaxation necessary for optimal surgery.

How does general anesthesia work on the brain?

The mechanisms of general anesthesia rely on targeted action on the central nervous system. When an anesthetic is administered intravenously or by inhalation, it causes a loss of consciousness, combined with insensitivity to pain and suspension of natural reflexes.

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This controlled disruption also involves the cessation of autonomous breathing and the suppression of airway reflexes. Consequently, tracheal intubation is often necessary to ensure artificial ventilation and maintain adequate oxygenation of the body. General anesthesia also alters the electrical activity of the brain, which can be measured by electroencephalography (EEG). A particular EEG pattern, called burst suppression, is characterized by alternating periods of cerebral electrical activity (bursts) and electrical silence (suppression). The propensity to develop burst suppression may be associated with low frontal alpha power on the EEG, suggesting a "vulnerable brain."

Post-anesthesia memory loss: a frequent side effect?

Memory loss following general anesthesia is a frequently observed phenomenon. This disorder, also known as postoperative cognitive dysfunction, can manifest variably in terms of duration and intensity.

Differences between temporary and long-term memory loss

There are two types of postoperative memory loss: temporary and long-term. In most cases, cognitive deficits are transient and fade within hours or days after the procedure. However, in some patients, especially the elderly, these disorders can persist for several months. It is estimated that up to 65% of patients aged 65 and over experience delirium and 10% develop long-term cognitive decline after non-cardiac surgery.

It is interesting to note that approximately one-third of patients undergoing surgery under general anesthesia experience cognitive impairment upon discharge from the hospital. Among them, one-tenth continue to experience the effects for up to three months after the operation.

Research highlights the fact that even low exposure to anesthetic agents can have prolonged repercussions on cognitive abilities. For example, studies conducted on mice have shown that the activity of receptors involved in memory loss remains elevated for several days after the administration of anesthetic substances, thus affecting their ability to learn and memorize.

Risk factors associated with memory loss after anesthesia

Among the factors that increase the risk of postoperative cognitive disorders, advanced age is the most prominent. Older people are indeed more likely to have lasting deficiencies. In addition, complex and major surgeries, such as thoracic or cardiac procedures, play a significant role. The type of intervention and the patient's overall health are also influencing factors. Older patients have age-related brain changes that can contribute to a decrease in cognitive reserve and an increased susceptibility to the stresses of surgery and anesthesia.

Repeated anesthetics can also amplify the risks. Tests on mice have shown that repeated administration of sevoflurane, a commonly used anesthetic gas, can lead to irreversible alterations in Tau proteins. These proteins are strongly associated with the neuronal degeneration observed in Alzheimer's disease, thus causing significant cognitive disorders.

Finally, certain perioperative events, such as hypoxemia or the use of medications complementary to anesthesia (such as benzodiazepines, central anticholinergics, meperidine, phenothiazines, and antipsychotics), can influence the occurrence and intensity of postoperative cognitive deficits. These perioperative factors must therefore be rigorously monitored to limit these adverse effects.

Studies and research on memory loss after general anaesthesia

Research on the cognitive effects of general anesthesia has provided a better understanding of the mechanisms that can lead to memory impairment in some patients. These in-depth analyses are essential for understanding these phenomena and improving the care of those affected.

Cases where memory loss has been observed

Memory loss is frequently observed in some patients after general anesthesia. For example, a study conducted by the Faculty of Medicine at the University of Toronto revealed that approximately one-third of patients undergoing surgery under general anesthesia experience cognitive impairment upon discharge from the hospital, including memory loss. Among them, approximately 10% continue to experience these disorders for up to three months after the procedure.

Another analysis published in the British Journal of Anaesthesia in 2018, involving almost 2,000 people over the age of 70, showed that exposure to surgery and general anaesthesia could affect the brain over the long term. Some patients thus suffered a subtle but noticeable decline in memory and thinking skills, highlighting the potential impact on cognitive functions.

More recently, research published in Scientific Reports in 2023 confirmed an increased risk of cognitive impairment after surgery under general anesthesia. These disorders sometimes appear to be correlated with structural changes in the brain, although further studies are needed to establish a concrete link. In addition, studies have suggested that anesthesia and surgery may be associated with a modest acceleration in the rate of cognitive decline in elderly patients and may potentially increase cerebral deposits of β-amyloid, a marker of Alzheimer's disease. A 2014 study observed an increased incidence of dementia and a reduced interval before diagnosis of dementia after anesthesia and surgery in patients aged 50 and over.

Limitations of existing studies

Although interesting, this research raises some questions. One of the main limitations lies in the difficulty of differentiating the factors involved: is it the anesthesia, the surgery, or the underlying pathologies that cause cognitive decline? It is difficult to determine with certainty whether the decline is related to the anesthesia itself or to other elements, such as pre-existing treatments or medical conditions.

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Furthermore, numerous studies have used mice to study the cognitive effects of anesthetics. A study conducted by Inserm showed that sevoflurane, administered repeatedly, causes alterations in Tau proteins and memory disorders. However, the direct transposition of these results to humans remains hypothetical.

To obtain precise and reliable answers, it is imperative to conduct prospective studies and in-depth long-term follow-ups. The current results, although significant, require confirmation and exploration in larger cohorts before reaching definitive conclusions.

Tips for minimizing the risk of memory loss

Reducing the risk of memory loss following general anaesthesia requires a structured approach before, during and after surgery. Several practical measures can be taken to optimize this process and improve patient comfort.

Preparation before an operation

The pre-anesthetic consultation plays an important role in preparation. This appointment allows for a detailed assessment of the patient's health status and a discussion of the different anesthesia options tailored to their needs. It is extremely important to report any history, such as intraoperative awareness, as well as any substances consumed that could alter the effectiveness of anesthetics, such as alcohol, opioids, antiepileptics, or benzodiazepines. A comprehensive preoperative evaluation should also address and optimize modifiable risk factors for postoperative neurocognitive disorders, such as functional status, frailty, hearing and vision impairments, depression, hypertension, sleep disorders, blood sugar, alcohol and other substance use, medications, nutritional status, and pain. Personalized prehabilitation programs and care pathways could also limit the incidence and severity of PND.

Adherence to pre-anesthetic fasting guidelines is also essential, as it helps prevent serious complications such as vomiting or pulmonary aspiration. Generally, it is recommended to avoid eating solid foods within six hours before the procedure, while allowing the consumption of liquids such as water, coffee or tea without milk, and pulp-free fruit juices, up to two hours before the operation.

Post-operative follow-up and recommendations

After the intervention, post-operative monitoring is a key step in quickly detecting and managing any disturbances in memory or concentration abilities. Patients should be informed of signs such as altered concentration, sleep disturbances or excessive drowsiness, and encouraged to consult their doctor if these symptoms persist. Screening for post-operative cognitive disorders, even silent ones, is essential and can be done using scores such as the CAM-ICU-7. The implementation of specific strategies based on screening and early management, with the support of families, the limitation of anticholinergic drugs and the early mobilization of patients, helps to reduce the impact of delirium and prevent its chronicity.

Sufficient rest after a general anaesthetic is highly recommended to allow the brain and body to recover fully. Although drugs are useless for directly counteracting anesthesia-related fatigue, vitamins can be suggested to facilitate overall recovery.

Finally, the use of combined anesthesia techniques, combining general anesthesia and regional anesthesia, represents an interesting alternative. This approach can reduce the depth of anesthesia and thus limit side effects. During the procedure, the use of advanced monitoring, such as the Bispectral Index (BIS), helps to precisely adjust the dosage of anesthetic agents. The BIS aims to avoid periods of "burst suppression" and the disappearance of alpha waves in spectral density on the monitor, as these two elements are correlated with a more frequent occurrence of postoperative cognitive disorders. Shao (4) suggests that BIS may also help to screen for "vulnerable brains" at greater risk of cognitive dysfunction. However, it is important to note that commercial algorithms for estimating burst suppression, such as BIS, may underestimate the actual duration of burst suppression compared to visual analysis of the EEG. Despite studies showing that intraoperative EEG monitoring guided by BIS may be associated with a decrease in postoperative delirium, other studies, such as the ENGAGES trial, have not shown a significant decrease in delirium. It is possible that a subgroup of cognitively frail patients may benefit from EEG-guided anesthetic depth. Raw EEG monitoring may be a better alternative for detecting and preventing burst suppression and postoperative delirium, with adequate training for practitioners.

Burst Suppression and Postoperative Cognitive Risk

Burst suppression on EEG during general anesthesia is being studied as a potential mechanism leading to postoperative cognitive impairment. Although studies present conflicting results, the current state of research suggests that burst suppression on EEG, its duration, and the trajectory of EEG emergence could predict postoperative delirium (POD). Several studies have shown that patients with intraoperative burst suppression on EEG had an increased risk of POD. In addition, a study on aortic surgeries found an association between lower BIS values (suggesting burst suppression) and an increased risk of POD and neurological events.

The exact mechanism of burst suppression is not fully understood, but two main hypotheses exist: the cortical hypersensitivity hypothesis and the metabolic hypothesis. EEG can also help identify "vulnerable brains" more likely to develop burst suppression and postoperative cognitive impairment. Studies have shown that advanced age, a history of coronary artery disease, and male sex may be risk factors for EEG suppression. In addition, low alpha and beta EEG power has been associated with older age, vulnerability to burst suppression, reduced cerebral metabolism, decreased cognitive abilities, and an increased risk of postoperative complications such as POD.

It is important to note that anesthetic agents can have different impacts on the EEG of patients and that the choice and dosage should be considered to avoid burst suppression. For example, halothane has minor effects on the EEG and does not cause burst suppression even at high doses. However, patients with increased sensitivity to volatile anesthetics and a history of smoking may experience EEG suppression at lower anesthetic concentrations and have a higher incidence of POD.

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