Interpreting EEG spectrograms (Density Spectral Arrays, DSA) during anesthesia is often seen as complex and challenging, especially when we combine several anesthetic agents like propofol, opioids, ketamine, lidocaine, dexmedetomidine,etc.

I have decided to compile and share with you some of my cases, but group them by type of surgery. This will simplify the information I saw.

This Visual Atlas was developed to provide a more tangible and relatable representation of DSA patterns. All cases were performed by the same anesthesiologist (myself), with the same surgical team, using a standardized TIVA protocol:

• Propofol bolus followed by continuous infusion.
• Remifentanil continuous infusion starting at 0.08 µg/kg/min.
• Ketamine: 0.2–0.3 mg/kg at the beginning of surgery.
• Lidocaine bolus at induction.
• Morphine (2–3 mg) at the beginning of surgery.
• Adjuvants: paracetamol, ondansetron, and dexamethasone

By maintaining a uniform technique and focusing on the same kind of surgery— laparoscopic cholecystectomy — this collection highlights how DSAs vary across different age groups and between men and women.

In younger patients, I did not find significant differences in DSA patterns between men and women. The most notable differences appear consistently after the age of 55 and in vulnerable brains.

The goal is not only to illustrate the EEG signatures of propofol, and what happened when we ad: remifentanil, and ketamine, etc… but also to stimulate reflection:

• Do we observe consistent gender-related differences?
• How does aging impact the density spectral array under identical anesthetic conditions?
• Can visual familiarity with these patterns lower the barrier to adopting EEG/DSA monitoring in daily practice?

This Atlas is shared as an educational resource — a step towards demystifying EEG interpretation and encouraging anesthesiologists to look beyond indices, into the living language of the brain.

I hope you find it useful and that you can also see what I am able to see in my patients.

@carolinafrederico

When I decide to teach a topic, prepare a lecture, create content for my website, or simply write a post about a complex article, I first ask myself if the message answers the question I want to address.
Because without a question, there’s no direction, and
Without direction, we are lost.

But what happens when you sit down at your computer and can’t find the question?

What happens when you reach a mental crossroads?

Imagine you wake up early in the morning with a long to-do list: prepare a class, study for an exam, update your website. But as soon as you sit in front of the screen, your mind goes blank.

At least not the kind of ideas I usually like: original, creative, and useful ideas that leave a mark and make people remember you because of them.
So why did this happen?

Is it just fatigue?
Are we overwhelmed?

I realized that when I feel lost and out of ideas, it’s usually because I’m dwelling on everything I’ve had to endure.

Each time I pause to reflect on my journey, I understand that my exhaustion doesn’t stem from today’s tasks; it stems from everything I’ve survived thus far.

All of that, along with being in spaces where what you do and what gets noticed don’t always match — starts to wear you down.

So when a day like this comes — a full schedule but no ideas — it’s not just exhaustion.
It’s a signal.
An uncomfortable pause that also invites something deeper.

What can we do when we reach that mental crossroads, unsure of what our purpose is?

Sometimes, the only thing we can do is stop.
Stop pushing.
And listen to the silence with the same care we usually give our ideas.

In the constant noise of producing, teaching, proving, and moving forward, we also need space to simply exist.

Maybe we won’t find the answer today.
But admitting that we don’t have it — that’s already an act of honesty.
In that moment, a new question may slowly begin to form.
And with it, a purpose that feels more real, more personal.
It may not always be brilliant or visible, but it will be true to what you believe in.

Remember:
It doesn’t matter how visible you are.
Or how many people recognize your work.
What truly remains over time is having stayed true to your values — without causing harm, without playing a double game.

Do good, without needing to be seen.
Do it with respect and humility, and most importantly, without stepping on anyone along the way.
Because, at the end of the day, quiet integrity is the only thing that truly lasts.

Happy summer to all!

— Carolina Frederico

In recent years, neuroscience has made significant progress in unraveling how neural networks generate different states of consciousness. We now know that consciousness does not depend on a single brain region, but rather emerges from the dynamic and coordinated interaction of multiple functional networks distributed throughout the brain (Mashour & Hudetz, 2018; Brown et al., 2011). This integration is essential for maintaining awareness, attention, and the ability to respond to our environment.

But what really happens when the brain is exposed to anesthetic agents? How do these functional networks, usually integrated and synchronized, become fragmented, leading to loss of consciousness? And even more intriguingly, how do they restore their connectivity and dynamics to allow recovery of consciousness? Exploring these mechanisms is not only fundamental for anesthetic safety, but also brings us closer to understanding the very nature of consciousness and its vulnerability to pharmacological intervention.

Current evidence indicates that anesthetic agents induce unconsciousness primarily by disrupting functional connectivity among large-scale brain networks, particularly affecting communication between the frontal and parietal cortices, as well as thalamocortical coupling (Brown et al., 2011; Mashour, 2014). This functional fragmentation results in the brain’s inability to integrate information, leading to a reversible loss of consciousness.

In this article, we will review:

• The main neural networks involved in consciousness (default mode network, central executive network, and salience network)
• How anesthetic agents alter the connectivity and dynamics of these networks
• The difference between connected and disconnected consciousness under anesthesia
• The clinical relevance of these findings for advanced monitoring and patient safety

The Neural Networks of Consciousness

Consciousness emerges from the dynamic interaction between several brain networks, primarily:

• Default Mode Network (DMN): Active during rest, introspection, and self-referential thought. Essential for autobiographical memory and internal thought processes.
• Central Executive Network (CEN): Involved in directed attention, working memory, and problem-solving. Enables adaptive responses to the environment.
• Salience Network (SN): Detects relevant stimuli and facilitates transitions between the DMN and CEN, regulating the balance between internal and external processes.

These networks are part of the so-called human connectome, the functional map of brain connections that enables the integration and processing of internal and external perceptions.

Functional Integration and Consciousness

Consciousness requires effective functional connectivity among these networks. The salience network acts as a mediator, determining when the brain should switch from an introspective state (DMN) to an active attention state (CEN), depending on the relevance of stimuli. The thalamus and thalamocortical connections are essential for synchronizing the activity of these networks and sustaining the conscious state.

Ultimately, conscious experience depends on the functional coordination of multiple neural networks. The action of anesthetic agents disrupts this coordination, causing a transient disconnection that manifests as loss of consciousness, without permanently altering brain architecture.

What Happens When We Administer Anesthetic Agents?

“General anesthesia is not a state of global brain suppression, but rather a state of altered connectivity among specific brain networks, particularly a breakdown in frontoparietal and thalamocortical connectivity.”
— Brown EN, Purdon PL, Van Dort CJ. (2011)

Connected and Disconnected Consciousness

States of consciousness can be classified as:

• Connected consciousness: Functional integration among networks, with conscious perception of the environment.
• Disconnected consciousness: Loss of connectivity, with absence of response to the environment, although internal experiences (such as dreams) may persist.

During anesthesia, the goal is to achieve a stable disconnected consciousness: no explicit memory, no pain, and autonomic stability. The EEG shows coherent frontal alpha-delta oscillations without spectral collapse, reflecting the stability of this state.

Effects of Anesthetic Agents on Neural Networks

Source: Adapted from Dr. Frederico conference, Barcelona 2025.

Feedforward, Feedback, and Consciousness

• Feedforward (ascending): Processing of information from sensory areas to frontal regions.
• Feedback (descending): Integration and prediction processing from frontal to sensory areas.

Anesthetic agents, especially propofol, preferentially block feedback (frontal ? parietal), leading to loss of integration and disconnection from external consciousness. Internal consciousness (DMN) may be partially preserved at low doses but becomes decoupled and silenced at surgical doses.

“Anesthetics preferentially disrupt top-down (feedback) connectivity, which is thought to be essential for conscious perception and integration.”
— Mashour GA. (2014)

Advanced Monitoring: EEG and DSA

Interpretation of EEG and the density spectral array (DSA) allows identification of specific patterns according to the anesthetic agent and state of consciousness. However, EEG-derived indices have limitations: they may omit the phenotypic richness of the EEG, do not anticipate rapid changes in consciousness, and do not account for individual variables such as age or frailty.

“The EEG signatures of general anesthesia reflect the underlying disruption of communication between brain regions, with specific patterns corresponding to different anesthetic agents and depths of anesthesia.”
— Purdon PL, Sampson A, Pavone KJ, Brown EN. (2015)

Clinical Implications

• Optimize monitoring of anesthetic depth.
• Anticipate and prevent cognitive complications, especially in vulnerable patients.
• Improve safety and quality of anesthetic care.

Conclusion

Understanding how anesthesia affects the brain is not just a scientific curiosity for me—it’s a responsibility. By clarifying these complex concepts, I hope to help my colleagues provide safer and more thoughtful care, because when we truly understand how consciousness is formed and how it can be disrupted, we are better able to safeguard our patients’ brains and improve their outcomes every day in the operating room.

References

1. Brown EN, Purdon PL, Van Dort CJ. General anesthesia and altered states of arousal: a systems neuroscience analysis. Annu Rev Neurosci. 2011;34:601-628. doi:10.1146/annurev-neuro-060909-153200.
2. Mashour GA, Hudetz AG. Neural Correlates of Unconsciousness in Large-Scale Brain Networks. Trends Neurosci. 2018;41(3):150-160. doi:10.1016/j.tins.2017.12.003.
3. Mashour GA. Top-down mechanisms of anesthetic-induced unconsciousness. Front Syst Neurosci. 2014;8:115. doi:10.3389/fnsys.2014.00115.
4. Purdon PL, Sampson A, Pavone KJ, Brown EN. Clinical Electroencephalography for Anesthesiologists: Part I: Background and Basic Signatures. Anesthesiology. 2015;123(4):937–960. doi:10.1097/ALN.0000000000000841.
5. Mashour GA. Integrating the Science of Consciousness and Anesthesia. Anesth Analg. 2019;128(4):783-789. doi:10.1213/ANE.0000000000004061.

Después de mucho trabajo, hoy te damos la bienvenida a una nueva etapa.
Rediseñamos este blog para que sea más claro, visual y —como siempre— 100% orientado a la práctica clínica y al pensamiento crítico.
En este espacio vas a encontrar:

? Videos, enlaces útiles y más

? Reflexiones breves sobre anestesia y neurociencia

? Explicaciones simples de conceptos complejos (EEG, DSA, TIVA…)

? Resúmenes comentados de artículos científicos

? Casos clínicos con interpretación

Este no es solo un blog cualquiera.
Es un espacio de encuentro para anestesiólog@s curios@s y apasionad@s como vos.

Gracias por ser parte de esta comunidad.
¡Seguimos pensando como cuidar a nuestros pacientes… juntos!

Con afecto,
Dra. Carolina Frederico

• 2 subunidades GluN1 (obligatorias),
• 2 subunidades GluN2 (A-D) o GluN3 (moduladoras).

Cada subunidad tiene varios dominios funcionales: el sitio de unión a ligando, el canal iónico y regiones de modulación alostérica.

Sitios de unión conocidos (principales y moduladores)

Aquí te dejo un resumen de lugares bien caracterizados donde actúan distintos ligandos:

¿Por qué esto importa?

Porque explica por qué el receptor NMDA:

• Responde de manera tan diversa a distintos anestésicos, iones, pH, y neuromoduladores.
• Tiene un rol central en procesos de plasticidad sináptica como LTP y LTD.
• Es un blanco clave no solo en anestesia, sino también en psiquiatría, dolor, neurodesarrollo y neurodegeneración.

¿Qué le hace el óxido nitroso al cerebro? Un vistazo desde el EEG

Aunque el óxido nitroso (N?O) no genera inconsciencia profunda por sí solo, sí produce efectos distintivos en el cerebro. Su mecanismo principal es el bloqueo de los receptores NMDA, pero su impacto es observable a gran escala… incluso en el EEG.

? Durante la transición hacia una mezcla con alta concentración de N?O (>70%), se observa algo curioso:
? una oleada transitoria de oscilaciones lentas-delta de gran amplitud, seguida por un patrón dominado por frecuencias beta y gamma.

Este fenómeno fue reportado por Emery Brown et al. y puede observarse claramente cuando se cambia de agentes como isoflurano a N?O con oxígeno:

Estas oscilaciones lentas transitorias no son las mismas que las del propofol o la dexmedetomidina. Se acompañan de una reducción marcada del poder en frecuencias >10 Hz, sugiriendo un cambio abrupto en la conectividad y excitabilidad cortical.

¿Cuál podría ser el mecanismo?

Una hipótesis planteada por los autores:

Estas ondas podrían deberse al bloqueo de entradas excitatorias NMDA-dependientes provenientes del núcleo parabraquial y la formación reticular.?

Es decir: al cortar de forma brusca estos inputs excitatorios, se impone un patrón de oscilaciones lentas y sincronizadas… como una especie de pausa funcional antes de que el cerebro reorganice su ritmo en beta-gamma.

Dato neuroanatómico para anestesiólogos
El núcleo parabraquial forma parte del sistema activador ascendente. Sus proyecciones glutamatérgicas ayudan a mantener el estado de alerta. Bloquear sus entradas —como ocurre con el óxido nitroso al inhibir NMDA— puede explicar los patrones EEG transitorios de oscilaciones lentas durante la emergencia anestésica.
? ¡La anatomía también habla en el EEG!

¿Por qué importa para nosotros?

Este cambio EEG revela que el óxido nitroso altera transitoriamente el modo en que las redes neuronales se comunican, y que su uso —especialmente en emergencia o transición anestésica— puede tener efectos más profundos de lo que parece.

La neuroplasticidad, el despertar y la integración de circuitos podrían estar siendo modulados, o incluso interrumpidos, por estas oscilaciones.

Mather et al. «Intraoperative Frontal Electroencephalogram Alpha Power Is Associated with Postoperative Mortality and Other Adverse Outcomes.» Anesthesiology 2025; 142:500–10.

The study suggests that lower intraoperative alpha power in the EEG is independently associated with increased postoperative mortality. While this is an intriguing hypothesis, I believe we must be cautious with these conclusions.

Critical Points to Consider

1. Lack of Information on Consciousness State Titration

The study reports anaesthetic doses, including

• Propofol median total dose: 200 mg (IQR 150-260 mg)
• Sevoflurane mean end-tidal concentration: 1.00% (IQR 0.00-1.39%)
• Nitrous oxide use: 60.3% of patients (a lot)

• Propofol mean total dose: 200 mg (IQR 150-260 mg)
• Sevoflurane mean end-tidal concentration: 1.00% (IQR 0.00-1.39%)
• Use of nitrous oxide: 60.3% of patients.
  
  However, it is not specified how the anaesthesia was titrated for each patient.
• No mention of burst suppression, a key indicator of excessive anaesthetic titration.
• No BIS, Entropy, Narcotrend, Conox monitoring, making it impossible to compare alpha power with other validated EEG monitoring data.
• No analysis of mean arterial pressure (MAP), so we cannot rule out cerebral hypoperfusion as a cause of reduced alpha power.

Without data on titration strategies, we cannot determine whether lower alpha power reflects patient frailty or simply excessive anesthesia administration.

2. Retrospective Study Design and Selection Bias

• This was a retrospective observational study, meaning it cannot establish causality, only statistical associations.
• Only patients with artifact-free EEG recordings were included, introducing selection bias.
• Other critical confounders (e.g., opioid use, neuromuscular blockade, ventilatory parameters) were not considered.

A prospective study is needed to validate these findings before drawing clinical conclusions.

3. Failure to Differentiate Between Patient Frailty and Over-Titration of Anesthesia

Low intraoperative alpha power could result from:
1. Pre-existing neurological frailty ? reduced cortical connectivity and baseline EEG activity.
2. Inadequate titration of consciousness state ? deeper hypnotic states leading to EEG suppression.
3. Cerebral hypoperfusion ? low MAP causing decreased cortical activity.

The study does not provide enough data to distinguish between these scenarios.

4 Unusual Anesthetic Practice: Predominance of Volatile Agents & Nitrous Oxide

One striking aspect of this study is the low use of total intravenous anesthesia (TIVA) and the high prevalence of volatile agents and nitrous oxide:

• 98.9% of patients received propofol, but only as an induction agent.
• 72.1% received sevoflurane as the primary anesthetic.
• 60.3% received nitrous oxide, a practice that has largely declined in LATAM and Europe due to concerns about environmental impact and neurotoxicity.

The study did not investigate whether the choice of anaesthesia influenced the EEG findings, and it could be questioned whether the findings would be the same in a cohort with predominantly intravenous anaesthesia.

5 No Comparison with Established Risk Prediction Models

• Several validated models predict postoperative mortality (ASA, POSSUM, ACS-NSQIP).
• This study does not compare alpha power with these models, making it unclear whether it adds predictive value.

Final Thoughts

At this stage, it is premature to consider intraoperative alpha power as an independent biomarker for mortality.
More rigorous, prospective studies are needed, incorporating Raw EEG/DSA, MAP, burst suppression analysis, and direct comparisons with existing risk models.

Additionally, the high use of volatile agents and nitrous oxide raises the question of whether these findings would hold true in a TIVA-based anesthesia protocol.

What are your thoughts on this? Have you encountered similar discussions in your practice?

Why Is Learning EEG Interpretation Essential for Personalized Anesthesia?

1  Optimized Drug Dosing for Each Patient

• EEG interpretation helps to adjust the anaesthetic to each patient’s needs, reducing the risk of under-dosing, which can lead to patient movement or inadequate anaesthesia, and over-sedation, which can delay recovery and increase complications.

2 Preventing Postoperative Delirium and Cognitive Dysfunction

• Over-sedation, particularly in older adults, is strongly associated with postoperative delirium and long-term cognitive impairment.
• EEG-guided anaesthetic titration helps prevent brain suppression (e.g. burst suppression patterns), reducing the risk of delirium and prolonging neurocognitive recovery..

3 Understanding the Effect of GABAergic Drugs on Thalamocortical Circuits

• Most general anaesthetics enhance GABAergic inhibition, which suppresses thalamocortical circuits and produces characteristic EEG changes.
• Moderate doses of anaesthetic often induce frontal alpha oscillations (8-12 Hz) reflecting synchronised inhibition of corticothalamic loops. This pattern is associated with stable unconsciousness.
• Deeper anaesthesia, particularly with excessive GABAergic activity, leads to high amplitude slow delta waves (0.5-4 Hz) and burst suppression, indicating profound cortical suppression and a greater risk of neurotoxicity and postoperative delirium.
• Understanding these variations in thalamocortical dynamics allows anaesthetists to assess whether a patient is adequately anaesthetised or receiving excessive suppression, which could affect postoperative recovery.

 4 Beyond Numerical Indices: A Deeper Understanding of EEG Data

• EEG-derived indices provide a numerical estimation of anesthetic depth, but their reliability varies based on factors such as age, medication type, and patient physiology.
• Complementing these indices with direct EEG interpretation enhances clinical decision-making, particularly in complex cases.
• Additional parameters, such as the Burst Suppression Index (BSI) and Alpha/Delta Ratio, can offer deeper insights into brain activity and help refine anesthetic management.

5 Personalized Anesthesia Through Neurophysiological Monitoring

• Each patient’s brain reacts uniquely to anesthesia. Real-time EEG monitoring allows for dynamic adjustments, reducing risks such as neurotoxicity in elderly patients, postoperative delirium, or insufficient sedation in younger populations.

The Future of EEG-Guided Personalized Anesthesia

Advancements in neuroscience and EEG technology are transforming anesthesia into a more precise and individualized practice. Learning to interpret EEG signals in real-time empowers anesthesiologists to fine-tune drug administration, optimize patient outcomes, and enhance overall surgical safety.

Are you integrating EEG interpretation into your anesthesia practice? Let’s discuss how real-time brain monitoring is shaping the future of personalized anesthesia.

Would you like to learn more about EEG in anesthesia? Share your thoughts and experiences in the comments! Let’s keep learning together.

La obesidad representa un desafío significativo en la práctica anestésica debido a las alteraciones en la fisiología del paciente con obesidad, especialmente a nivel respiratorio, cardiovascular y metabólica. En este contexto, la Anestesia Total Intravenosa (TIVA) se presenta como una alternativa atractiva a la anestesia inhalatoria, ofreciendo ventajas como una recuperación más predecible, menor contaminación ambiental y una reducción en la incidencia de náuseas y vómitos postoperatorios (PONV). Sin embargo, su uso en este tipo de pacientes requiere un entendimiento profundo de la farmacocinética y farmacodinámica de los fármacos utilizados.

1. Principales desafíos anestésicos en el paciente obeso

Los anestesiólogos enfrentan múltiples preocupaciones al manejar un paciente con obesidad, entre ellas:

• Vía aérea difícil: La obesidad se asocia con mayor incidencia de ventilación difícil con mascarilla, intubación complicada y riesgo de desaturación rápida debido a la disminución de la capacidad residual funcional (CRF).
• Distribución y metabolismo de los anestésicos: La dosificación/titulación de fármacos es compleja debido a la alteración en el volumen de distribución y el metabolismo hepático. La elección del peso corporal ideal (IBW), peso magro (LBW) o peso ajustado (ABW) en lugar del peso total (TBW) puede optimizar la administración de fármacos como el propofol y los opioides.
• Ventilación intraoperatoria: El aumento en la resistencia de la pared torácica y el abdomen puede llevar a hipoventilación, atelectasias e hipoxemia. Se recomienda el uso de PEEP y maniobras de reclutamiento alveolar para mejorar la oxigenación.
• Recuperación postoperatoria: Mayor riesgo de apnea obstructiva del sueño (AOS), hipercapnia postoperatoria, retención de anestésicos y complicaciones tromboembólicas.

2. ¿Por qué TIVA en el paciente obeso?

El uso de la técnica TIVA con un abordaje multimodal, ofrece varias ventajas sobre la anestesia inhalatoria:

• Rápida Recuperación
• Menor riesgo de PONV, lo que favorece una recuperación más rápida.
• Evita el uso de agentes volátiles y gases halogenados, reduciendo contaminación ambiental.
• Menor alteración en la mecánica respiratoria, ya que los anestésicos inhalatorios pueden potenciar la depresión respiratoria.
• Menor riesgo de hipertermia maligna, condición más difícil de manejar en obesos.

Sin embargo, para obtener estos beneficios, es fundamental ajustar correctamente las dosis y elegir el modelo de administración adecuado.

3. ¿Cómo dosificar propofol en obesos?

El propofol es altamente lipofílico y su volumen de distribución aumenta en pacientes obesos. Para evitar sobredosis o recuperación prolongada, se recomienda calcular la dosis según:

• Inducción: Peso ajustado (ABW), corporal magro (LBW) en lugar de peso total (TBW).
• Mantenimiento: Uso de modelos alométricos de TCI (Target-Controlled Infusion) como como Eleveld, Cortínez o se puede usar Schnider o Marsh con Peso Ajustado y guiado por monitores de EEG no procesado (BIS, SEDLine, NINDEX, Narcotrend, Entropía, Conox).
• También es válido hacer TIVA Manual usando Peso ajustado y guiado por EEG

4. Estrategia de administración: ¿Manual o TCI?

TIVA Manual (Bolo + infusión ajustada clínicamente)

• Fácil de implementar sin necesidad de bombas con software TCI.
• Mayor riesgo de infra o sobredosificación.

TIVA con TCI (Infusión Controlada por Objetivo)

• Permite administración precisa y mantiene niveles estables de propofol.
• Reduce la variabilidad interindividual en obesos.
• Evita acumulación innecesaria del fármaco.

5. ¿Libre de opioides en obesos? (OFA, Opioid-Free Anesthesia)

El uso de TIVA libre de opioides (OFA) en obesos es un tema en evolución. Algunas ventajas de evitar opioides incluyen:

• Menor riesgo de depresión respiratoria postoperatoria.
• Disminución del impacto en la función gastrointestinal.
• Reducción en la hiperactividad simpática.

Sin embargo, la analgesia multimodal debe ser optimizada con dexmedetomidina, lidocaína, ketamina, AINEs y bloqueos nerviosos para evitar déficit analgésico.

Conclusión

El manejo de TIVA en pacientes con obesidad requiere un enfoque basado en la farmacocinética y farmacodinámica de los agentes anestésicos.

• Ajustar las dosis en base al descriptor de peso adecuado.
• Utilizar TCI para evitar infra o sobredosificación.
• Evaluar la viabilidad de una estrategia libre de opioides (OFA) según el tipo de cirugía y comorbilidades.

? ¡Queremos conocer tu experiencia! Responde este breve cuestionario sobre cómo manejas la TIVA en obesos

? https://forms.gle/kHjTd8AECW5g4zH39

Recuerda que estaremos abordandomelas este el tema de la Obesidad en distintos escenarios clínicos en la 3ra Jornada Iberoamericana de TIVA y Neurociencias, el 30 y 31 de mayo en Barcelona.