Artificial intelligence has been advancing in fields including anesthesiology. This scoping review of the intersection of artificial intelligence and anesthesia research identified and summarized six themes of applications of artificial intelligence in anesthesiology: (1) depth of anesthesia monitoring, (2) control of anesthesia, (3) event and risk prediction, (4) ultrasound guidance, (5) pain management, and (6) operating room logistics. Based on papers identified in the review, several topics within artificial intelligence were described and summarized: (1) machine learning (including supervised, unsupervised, and reinforcement learning), (2) techniques in artificial intelligence (e.g., classical machine learning, neural networks and deep learning, Bayesian methods), and (3) major applied fields in artificial intelligence. The implications of artificial intelligence for the practicing anesthesiologist are discussed as are its limitations and the role of clinicians in further developing artificial intelligence for use in clinical care. Artificial intelligence has the potential to impact the practice of anesthesiology in aspects ranging from perioperative support to critical care delivery to outpatient pain management.

Background: Electroencephalogram patterns observed during sedation with dexmedetomidine appear similar to those observed during general anesthesia with propofol. This is evident with the occurrence of slow (0.1 to 1 Hz), delta (1 to 4 Hz), propofol-induced alpha (8 to 12 Hz), and dexmedetomidine-induced spindle (12 to 16 Hz) oscillations. However, these drugs have different molecular mechanisms and behavioral properties and are likely accompanied by distinguishing neural circuit dynamics. Methods: The authors measured 64-channel electroencephalogram under dexmedetomidine (n = 9) and propofol (n = 8) in healthy volunteers, 18 to 36 yr of age. The authors administered dexmedetomidine with a 1-µg/kg loading bolus over 10 min, followed by a 0.7 µg kg⁻¹ h⁻¹ infusion. For propofol, the authors used a computer-controlled infusion to target the effect-site concentration gradually from 0 to 5 μg/ml. Volunteers listened to auditory stimuli and responded by button press to determine unconsciousness. The authors analyzed the electroencephalogram using multitaper spectral and coherence analysis. Results: Dexmedetomidine was characterized by spindles with maximum power and coherence at approximately 13 Hz (mean ± SD; power, −10.8 ± 3.6 dB; coherence, 0.8 ± 0.08), whereas propofol was characterized with frontal alpha oscillations with peak frequency at approximately 11 Hz (power, 1.1 ± 4.5 dB; coherence, 0.9 ± 0.05). Notably, slow oscillation power during a general anesthetic state under propofol (power, 13.2 ± 2.4 dB) was much larger than during sedative states under both propofol (power, −2.5 ± 3.5 dB) and dexmedetomidine (power, −0.4 ± 3.1 dB). Conclusion: The results indicate that dexmedetomidine and propofol place patients into different brain states and suggest that propofol enables a deeper state of unconsciousness by inducing large-amplitude slow oscillations that produce prolonged states of neuronal silence.

Background: A clear understanding of the neural basis of consciousness is fundamental to research in clinical and basic neuroscience disciplines and anesthesia. Recently, decreased efficiency of information integration was suggested as a core network feature of propofol-induced unconsciousness. However, it is unclear whether this finding can be generalized to dexmedetomidine, which has a different molecular target. Methods: Dexmedetomidine was administered as a 1-μg/kg bolus over 10 min, followed by a 0.7-μg · kg⁻¹ · h⁻¹ infusion to healthy human volunteers (age range, 18 to 36 yr; n = 15). Resting-state functional magnetic resonance imaging data were acquired during baseline, dexmedetomidine-induced altered arousal, and recovery states. Zero-lag correlations between resting-state functional magnetic resonance imaging signals extracted from 131 brain parcellations were used to construct weighted brain networks. Network efficiency, degree distribution, and node strength were computed using graph analysis. Parcellated brain regions were also mapped to known resting-state networks to study functional connectivity changes. Results: Dexmedetomidine significantly reduced the local and global efficiencies of graph theory–derived networks. Dexmedetomidine also reduced the average brain connectivity strength without impairing the degree distribution. Functional connectivity within and between all resting-state networks was modulated by dexmedetomidine. Conclusions: Dexmedetomidine is associated with a significant drop in the capacity for efficient information transmission at both the local and global levels. These changes result from reductions in the strength of connectivity and also manifest as reduced within and between resting-state network connectivity. These findings strengthen the hypothesis that conscious processing relies on an efficient system of information transfer in the brain.

Objective: Delirium is a complex neurocognitive syndrome suspected to be bidirectionally linked to dementia. Circadian rhythm disturbances likely contribute to dementia pathogenesis, but whether these disturbances are related to delirium risk and progression to all‐cause dementia is unknown.Methods: We analyzed continuous actigraphy data from 53,417 middle‐aged or older UK Biobank participants during a median 5 years of follow‐up. Four measures were used to characterize the 24‐hour daily rest–activity rhythms (RARs): normalized amplitude, acrophase representing the peak activity time, interdaily stability, and intradaily variability (IV) for fragmentation of the rhythm. Cox proportional hazards models examined whether RARs predicted incident delirium (n = 551) and progression to dementia (n = 61).Results: Suppressed 24‐hour amplitude, lowest (Q1) versus highest (Q4) quartile (hazard ratio [HR]_{Q1 vs Q4}= 1.94, 95% confidence interval [CI] = 1.53–2.46,p < 0.001), and more fragmented (higher IV: HR_{Q4 vs Q1}= 1.49, 95% CI = 1.18–1.88,p < 0.001) rhythms predicted higher delirium risk, after adjusting for age, sex, education, cognitive performance, sleep duration/disturbances, and comorbidities. In those free from dementia, each hour of delayed acrophase was associated with delirium risk (HR = 1.13, 95% CI = 1.04–1.23,p = 0.003). Suppressed 24‐hour amplitude was associated with increased risk of progression from delirium to new onset dementia (HR = 1.31, 95% CI = 1.03–1.67,p = 0.03 for each 1‐standard deviation decrease).Interpretation: Twenty‐four‐hour daily RAR suppression, fragmentation, and potentially delayed acrophase were associated with delirium risk. Subsequent progression to dementia was more likely in delirium cases with suppressed rhythms. The presence of RAR disturbances before delirium and prior to progression to dementia suggests that these disturbances may predict higher risk and be involved in early disease pathogenesis. ANN NEUROL 2023;93:1145–1157

More random fluctuations in daily motor activity predict deteriorated quality of life and high death rate in elderly subjects.