Anesthetized

Upon completion of these surgical procedures, the incision was closed with sutures and treated with antibiotic cream. Eyes were kept lubricated with sterile saline applied at the beginning of the wait period for anesthesia stabilization , and vital signs were monitored throughout recording. Any effect from ketamine administered during induction was minimal as multiple hours elapsed prior to the start of electrophysiological recordings, and the elimination half-life of ketamine has been reported to be 45—60 min Davidson and Plumb General anesthesia was maintained with iso 0.

Intravenous access was established in the cephalic vein, and fluids included 4. To optimize electrophysiological stability, 0. The temporal order of iso concentrations was randomized across animals to control for changes related to continuous infusion of xylazine.

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At least 20 min elapsed after changing anesthetic concentration prior to starting a new recording, exceeding the amount of time required in our setup for the LFP to stabilize at the new anesthetic concentration. We were interested in assessing differences in sensory-evoked activity over a range of anesthetic depths that each maintained general anesthesia. Informally in the course of pilot experiments, all dosing achieved loss of the righting reflex, but systematic assessment during the recordings was technically not feasible. The dosing used did not induce long periods of isoelectric brain activity.

For channel probes, the reference electrode was located on the same shank 0. Probes were slowly advanced into cortex using a micromanipulator Narishige, Tokyo, Japan , and correct depth was determined online by small deflections of the LFP at superficial electrode recording sites and larger deflections of the LFP at deeper electrode recording sites.

Current source density CSD analysis was performed offline to verify electrode positioning across cortical layers Fig. CSD was determined by calculating the second spatial derivative of the low-pass filtered and smoothed LFP in response to full-field flashes presented at a rate of 1 Hz Ulbert et al.

Upon correct depth placement of the electrode s , the animal was presented with visual or auditory stimuli. The same stimuli were presented to awake and anesthetized animals. The same monitor and animal positions were used across sessions, for both awake and anesthetized animals. Correct timing of individual display frames was ascertained by a photodiode covering a small flashing square in the corner of the monitor. This visual stimulus was part of a larger set of stimuli that was presented during each recording session in randomized order.

The checkerboard visual stimulus enabled the study of responses to both abrupt transitions i. Receptive field mapping was conducted to functionally verify recording location in V1 Fig. Each square was shown for 30 repeats of each color in a randomized presentation order. MUA evoked by each square was calculated by subtracting baseline MUA during the 50 ms immediately prior to the stimulus onset from MUA 30—80 ms after stimulus onset. Based on comparable receptive field maps across recordings, consistent craniotomy and electrode insertion locations, and unchanged animal and monitor position, we are confident of consistent visual stimulation across recording sessions.

We validated our PFC recording locations by histological verification of probe location recording probe dipped in DiI, Invitrogen, Grand Island, NY, before insertion to ensure the electrode was properly inserted in the rostral portion of the anterior sigmoid gyrus Duque and McCormick , 2 mm from the midline Fig. Auditory stimulation trial structure was similar to visual stimulation We used a microphone to record sound on a channel of our electrophysiology recording system during the entirety of auditory stimulation sessions. We applied a threshold to this auditory signal channel to detect the onset of stimulation and synchronize the presentation of auditory stimuli with neural recordings.

During awake recordings, continuous infrared video recording Handycam, HDR-cxv, Sony, Tokyo, Japan was used to document that the animal was awake, as evidenced by open eyes, whisking, and nose twitching. Two of the awake animals one each: V1 and PFC recording locations were subsequently used for anesthetized recordings to minimize the total number of animals used in this study.

Presented anesthetized data were combined across both sets of animals. For experimental feasibility, single metal electrodes were used to acquire electrophysiological data instead of multichannel probes. Electrophysiological signals were recorded using single metal electrodes acutely inserted in putative layer IV, measured 0.

A silver chloride wire tucked between the skull and soft tissue was used as the reference. All other details of the surgical and experimental procedures were the same as described above. For some depth probes, a few select channels had to be excluded because of known defects in Neuronexus B-stock probes; in these cases, we interpolated data from neighboring channels. If not stated otherwise, the mean across recording sites and trials was calculated per recording session, and figures represent means across recording sessions number of recording sessions, visual stimulation: Laminar probes and CSD allowed for analysis of responses by layers: Varying iso levels were collapsed for the analysis of PFC and the response to auditory stimulation.

The distribution of thresholds for awake recordings was within the range of thresholds obtained in anesthetized recordings. For response histograms, spiking rate was calculated based on ms bins. Time constants were calculated by fitting an exponential with offset to the MUA response for the time periods indicated: MU response latency was calculated from histograms with 5-ms bins for increased temporal resolution.

Time-dependent frequency content was determined by convolution of the raw extracellular voltage signals with a family of Morlet wavelets 0. The same methods were applied to recordings from awake and anesthetized animals. All spectra are shown on a logarithmic scale. The power enhancement ratio was calculated as the ratio between spectral power during visual stimulation to spectral power during spontaneous activity before stimulation.

Spike-triggered averages from 1-s segments of LFP around each spike were obtained. Multitaper spectral estimates were used to determine spectra of the spike-triggered averages MATLAB pmtm function with time-bandwidth product of 3. Multitaper spectral analysis was used because this approach is optimized for spectral analysis of short data segments such as those obtained from data surrounding each spike time and is well-suited for nonstationary signal with rapid fluctuations van Vugt et al.

SFC values were given by the ratio of spike-triggered average spectra to the average of spectra calculated from each LFP segment Fries et al. Thus SFC is normalized for spike rate and spectral power. These values were calculated per channel, and statistics were conducted across sessions. Normalization was conducted by subtracting the average ITPC during full-field dark screen visual stimulation or silence auditory stimulation. Recordings conducted under all doses of anesthetics were combined.

We defined a region of interest ROI of 0. While a commonly applied metric to assess phase-resetting, evidence suggests that ITPC may also reflect evoked responses. To test for this, we utilized the methods proposed by Martinez-Montes et al. Specifically, we calculated the t-like statistic, which assesses if there is a significant difference between the sample mean of the wavelet coefficients for each time point and frequency and the average of these sample means for the prestimulus period.

A local false discovery rate of 0. To gain insight into the functional connectivity between V1 and PFC, the time-dependent spectral coherence was estimated by first convolving the raw signal in V1 and PFC with a family of Morlet wavelets across frequencies 0. For each trial, the auto spectra in V1 and PFC and the cross spectrum were calculated. The auto spectra in V1, auto spectra in PFC, and cross spectrum were averaged across trials, without smoothing within trials. The time-frequency spectral coherence was then calculated as the square of the averaged cross spectrum, normalized by the product of the averaged auto spectra from V1 and PFC Zhan et al.

This method of calculating coherence does not assume a stationary signal. Spectral coherence was calculated per recording session, and means were calculated across sessions to provide group-averaged results. Time-averaged spectral coherence was obtained by averaging over time during presentation of the visual stimulus. This coherence measure assumes a linear dependence of activity between V1 and PFC and takes values from 0 absent coherence to 1 perfect coherence.

Since the functional relationship of V1 and PFC activity is not well-understood and the assumption of linear dependency may not hold, we additionally calculated nonlinear phase-locking between V1 and PFC Lachaux et al. The circular variance of the phase differences between V1 and PFC was computed over trials in each recording and then averaged across recordings to provide the group-averaged phase-locking value V1-PFC PLV. Tukey's honestly significant difference criterion was used to correct for multiple comparisons.

To elucidate how micro- and mesoscale network dynamics of sensory processing differ between awake and anesthetized animals, we performed multichannel electrophysiology combined with sensory stimulation in head-fixed ferrets Fig. The visual stimulus 10 s consisted of 10 frozen-noise, static checkerboard patterns that were consecutively presented at a frequency of 1 Hz Fig.

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These two cortical recording locations were chosen to capture responses in and interactions between a primary sensory area and a higher-order cortical association area. We used multichannel depth probes for simultaneous electrophysiological recordings from all cortical layers [ Fig. Receptive field mapping demonstrated well-defined visual responses and, therefore, provided functional verification of recording location in V1 Fig.

Infrared videography was used to verify that animals were awake for the entirety of the awake recordings, as determined by the presence of whisking, minor movements, and blinking. Animals had not been trained in any task and were freely viewing during the recordings. In one conceptual framework, anesthetics could selectively alter information flow between higher-order cortical areas and spare processing in primary sensory cortices, leaving sensory responses intact.

Alternatively, anesthesia could indiscriminantly suppress visual responses and, therefore, reduce overall representation of sensory input. Lastly, anesthetics could disrupt specific aspects of the spatio-temporal response dynamics in the cortical microcircuit. To disambiguate between these possibilities, we first asked if and how visual responses in V1 measured by MUA were altered during anesthesia. We found that MUA responses differed strikingly between recordings in the awake and anesthetized animal. Importantly, we did not find broad suppression of visual responses by anesthetics.

Rather, we identified several pronounced differences in the temporal structure of MUA responses between awake and anesthetized animals. In the awake animal, MUA response dynamics exhibited two salient features. First, in response to the onset of the s visual stimulus, a strong MUA response occurred Fig. MU responses markedly decreased with subsequent transitions to the next checkerboard pattern within each trial of the s visual stimulus Figs. Second, awake animals exhibited temporally precise, transient increases in MUA in response to each transition in the stimulus Fig.

In anesthetized animals, the amplitude of visually-evoked MUA was comparable for the stimulus onset and the subsequent noise-pattern transitions in the stimulus Fig. Accordingly, the decay time constant for the MUA response was significantly longer in anesthetized animals compared with that in awake animals [ Fig. Representative MUA responses in awake and anesthetized animals. Awake animals exhibited MUA primarily at stimulus onset and the first few transitions of noise patterns.

In anesthetized animals, MUA was strongly driven by the stimulus transitions for the entire duration of the visual stimulation. Red bars indicate presentation times of the visual stimulus. Blue lines indicate threshold for extracting spikes; both large amplitude spikes and small amplitude spikes were extracted. MU spike-time histograms from a single recording session for an awake animal left and an animal anesthetized with 1.

Raw traces shown in A are from these recording sessions. Large red arrows indicate stimulus onset and offset; small red arrows indicate transitions between noise patterns in the stimulus. Differences in MUA response dynamics between awake and anesthetized animals. MUA exhibited a shorter decay time constant in awake animals compared with anesthetized animals. Red line, exponential fit of decay time course. All plots show averages across cortical layers. Five-millisecond binning was used for finer temporal resolution. Red lines, stimulus onset.

Response latency was not significantly different between awake and anesthetized animals. Error bars indicate 1 SE. We calculated MU firing rate using 5-ms bins to provide better temporal resolution at the onset of the visual stimulus but found no alteration in the response latency of MU firing Fig. The latency of MU spiking after onset of the visual stimulus exhibited a significant group factor of condition awake, 0.

Together, these results indicate that anesthetics altered V1 visually-evoked spiking by maintaining a large-amplitude response to each subsequent transition in the stimulus and concomitantly inducing prolonged MUA responses to transients in the visual input. Previous work has demonstrated that anesthetics selectively alter spontaneous activity as a function of cortical layer Sellers et al.

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We here sought to investigate if MUA responses to visual input also differed across cortical layers during anesthesia. Understanding the impact of anesthetics on dynamics across layers in the cortical microcircuit is particularly tractable in V1 because of the well-established pathway of information flow between cortical layers in visual processing Binzegger et al. Thirty-two-channel depth probes allowed for simultaneous acquisition of electrophysiological activity across all cortical layers Fig.

In awake animals, there was a trend level difference in visually-evoked spiking rates across cortical layers Fig. For the three levels of anesthetic, there were significant and trend level effects of cortical layer on increased visually-evoked spiking, particularly with differences in the granular layer Fig. Disruption of the laminar distribution and adaptation of visually-evoked MUA responses. Compared with awake animals top , increasing concentrations of anesthetic bottom ; 0.

Awake animals exhibited slightly higher MU firing rate in granular and infragranular layers compared with supragranular layers. Awake animals exhibited pronounced spike rate adaptation for later noise patterns, while anesthetics slowed this adaptation of MUA. Given this trending increase in MUA response in the granular layer during anesthesia, we next asked if anesthetics altered adaptation dynamics to the 1-Hz temporal structure of the stimulus as a function of cortical depth.

In awake animals, we observed adaptation of supragranular, granular, and infragranular layers to repeated presentations of the stimulus Fig. During anesthesia, this adaptation of MUA responses was slowed; supragranular, granular, and infragranular layers each exhibited inconsistent modulation in response across the 10 transitions between checkerboard-noise patterns within the visual stimulus Fig. Decreased activity in the main output layer layer V, infragranular layers relative to activity in the input layer layer IV, granular layers suggests that the interaction between cortical areas may be impaired under anesthesia.

Given these changes in the temporal activity structure of microscopic sensory responses measured by MUA, we next asked if mesoscopic activity patterns, in particular the frequency structure of the LFP, were also altered by anesthetics. During visual stimulation in awake animals, the LFP Fig. In contrast, in anesthetized animals, spectral power was predominantly driven by the temporal patterning of the visual stimulus Fig.

To assess if this difference in spectral modulation was limited to certain cortical layers, we determined stimulation-induced modulation of spectral power by cortical layer Fig. Indeed, we found similar response profiles across layers; in addition, in both awake and anesthetized animals, spectral modulation at low frequencies was greater in granular and infragranular layers compared with supragranular layers. We next quantified the enhancement of power in each frequency band by the visual stimulus, by calculating the ratio of power during visual stimulation to power during spontaneous activity before stimulation.

Visual stimulation enhanced power for frequency bands in both awake and anesthetized animals, with the greatest enhancement at the highest concentrations of iso Fig. Enhancement in each frequency band for animals anesthetized with 0. In addition, post hoc tests demonstrated that delta, theta, alpha, and beta power enhancement were significantly different between 0. Thus increasing concentrations of iso increased power across all frequency bands, but with the greatest enhancement in the lower frequency bands and in granular and infragranular layers.

Representative LFP responses to visual input in V1. Red bars indicate presentation of visual stimulus. Plots show averages across cortical layers. Differences in mesoscale LFP responses to visual input in V1. In both awake left and 1. In both awake and anesthetized animals 0. Greater enhancement in power was evident as iso concentration increased. Given the prolonged MUA responses to visual stimulation, together with the broad-band increases in stimulus-driven frequency structure during anesthesia, we asked how the functional interaction between microscopic and mesoscopic network dynamics was modulated by anesthetics.

We found that SFC was minimal in awake animals, while anesthetics induced differential effects based on cortical layer Fig. To further quantify the frequency and layer specificity of changes in SFC during anesthesia, we developed a metric to indicate the relative enhancement of low-frequency SFC Fig. With anesthetic, the SFC ratio increased for supragranular Fig. These results demonstrate that, during anesthesia, there was increased synchronization of the LFP and spiking activity, preferentially at lower frequencies.

Given the likely role of mesoscale dynamics measured by the LFP in enabling and timing the interaction between cortical areas, we next investigated the effects of anesthetics on functional cortical connectivity. Anesthetics increased spike-field coherence SFC in V1 during visual stimulation, preferentially at low frequencies. This figure shows group-averaged SFC by cortical depth during presentation of visual stimulation.

SFC was low in awake animals across cortical layers. Specifically, compared with awake animals, anesthetized animals exhibited increased SFC in supragranular and infragranular layers, increased SFC at low frequencies in granular layers, and decreased SFC at higher frequencies in granular layers. Putative granular layer IV electrode depth 0. Motivated by the evidence for prominent changes in the magnitude, duration, and adaptation of visually-evoked responses in V1 by anesthetics, we next asked if representation of the visual input in PFC was also altered by anesthetics.

If anesthetic agents cause functional disconnectivity of cortico-cortical circuits, PFC responses to sensory stimulation present in the awake animal should be absent in the anesthetized animal. To quantify this difference between the awake and anesthetized animals, we defined a ROI of 0. The physiologic effects are much greater when the block is placed above the 5th thoracic vertebra.

An ineffective block is most often due to inadequate anxiolysis or sedation rather than a failure of the block itself. Pain that is well managed during and immediately after surgery improves the health of patients by decreasing physiologic stress and the potential for chronic pain. Instead, it is a dynamic process wherein persistent painful stimuli can sensitize the system and either make pain management difficult or promote the development of chronic pain. Pain management is classified into either pre-emptive or on-demand. On-demand pain medications typically include either opioid or non-steroidal anti-inflammatory drugs but can also make use of novel approaches such as inhaled nitrous oxide [13] or ketamine.

PCA has been shown to provide slightly better pain control and increased patient satisfaction when compared with conventional methods. It reduces the duration of postoperative tracheal intubation by roughly half. The occurrence of prolonged postoperative mechanical ventilation and myocardial infarction is also reduced by epidural analgesia. Risks and complications as they relate to anesthesia are classified as either morbidity a disease or disorder that results from anesthesia or mortality death that results from anesthesia.

Quantifying how anesthesia contributes to morbidity and mortality can be difficult because a person's health prior to surgery and the complexity of the surgical procedure can also contribute to the risks. Prior to the introduction of anesthesia in the early 19th century, the physiologic stress from surgery caused significant complications and many deaths from shock. The faster the surgery was, the lower the rate of complications leading to reports of very quick amputations.

The advent of anesthesia allowed more complicated and life-saving surgery to be completed, decreased the physiologic stress of the surgery, but added an element of risk. It was two years after the introduction of ether anesthetics that the first death directly related to the use of anesthesia was reported. There is usually overlap in the contributing factors that lead to morbidity and mortality between the health of the patient, the type of surgery being performed and the anesthetic.

To understand the relative risk of each contributing factor, consider that the rate of deaths totally attributed to the patient's health is 1: Compare that to the rate of deaths totally attributed to surgical factors 1: These statistics can also be compared to the first such study on mortality in anesthesia from , which reported a rate of death from all causes at 1: Rather than stating a flat rate of morbidity or mortality, many factors are reported as contributing to the relative risk of the procedure and anesthetic combined.

For instance, an operation on a person who is between the ages of 60—79 years old places the patient at 2. Having an ASA score of 3, 4 or 5 places the person at Other variables include age greater than 80 3. The immediate time after anesthesia is called emergence. Emergence from general anesthesia or sedation requires careful monitoring because there is still a risk of complication.

There is a need for airway support in 6. Hypothermia , shivering and confusion are also common in the immediate post-operative period because of the lack of muscle movement and subsequent lack of heat production during the procedure. Postoperative cognitive dysfunction also known as POCD and post-anesthetic confusion is a disturbance in cognition after surgery.

It may also be variably used to describe emergence delirium immediate post-operative confusion and early cognitive dysfunction diminished cognitive function in the first post-operative week. Andrew Hudson, an assistant professor in anesthesiology states, "Recovery from anesthesia is not simply the result of the anesthetic 'wearing off,' but also of the brain finding its way back through a maze of possible activity states to those that allow conscious experience. Put simply, the brain reboots itself. Long-term POCD is a subtle deterioration in cognitive function, that can last for weeks, months, or longer.

Most commonly, relatives of the person report a lack of attention, memory and loss of interest in activities previously dear to the person such as crosswords. In a similar way, people in the workforce may report an inability to complete tasks at the same speed they could previously.

anesthetize

POCD also appears to occur in non-cardiac surgery. Its causes in non-cardiac surgery are less clear but older age is a risk factor for its occurrence. The first attempts at general anesthesia were probably herbal remedies administered in prehistory. Alcohol is one of the oldest known sedatives and it was used in ancient Mesopotamia thousands of years ago. The ancient Egyptians had some surgical instruments, [32] [33] as well as crude analgesics and sedatives, including possibly an extract prepared from the mandrake fruit.

Pien Ch'iao , c. Throughout Europe, Asia, and the Americas a variety of Solanum species containing potent tropane alkaloids were used for anesthesia. In 13th-century Italy, Theodoric Borgognoni used similar mixtures along with opiates to induce unconsciousness, and treatment with the combined alkaloids proved a mainstay of anesthesia until the nineteenth century.

Local anesthetics were used in Inca civilization where shamans chewed coca leaves and performed operations on the skull while spitting into the wounds they had inflicted to anesthetize. It was first used in by Karl Koller , at the suggestion of Sigmund Freud , in eye surgery in Early Arab writings mention anesthesia by inhalation. This idea was the basis of the "soporific sponge" "sleep sponge" , introduced by the Salerno school of medicine in the late twelfth century and by Ugo Borgognoni — in the thirteenth century.

The sponge was promoted and described by Ugo's son and fellow surgeon, Theodoric Borgognoni — In this anesthetic method, a sponge was soaked in a dissolved solution of opium, mandragora , hemlock juice, and other substances. The sponge was then dried and stored; just before surgery the sponge was moistened and then held under the patient's nose. When all went well, the fumes rendered the patient unconscious. The most famous anesthetic, ether , may have been synthesized as early as the 8th century, [39] [39] [40] but it took many centuries for its anesthetic importance to be appreciated, even though the 16th century physician and polymath Paracelsus noted that chickens made to breathe it not only fell asleep but also felt no pain.

By the early 19th century, ether was being used by humans, but only as a recreational drug. Meanwhile, in , English scientist Joseph Priestley discovered the gas nitrous oxide. Initially, people thought this gas to be lethal, even in small doses, like some other nitrogen oxides. However, in , British chemist and inventor Humphry Davy decided to find out by experimenting on himself. To his astonishment he found that nitrous oxide made him laugh, so he nicknamed it "laughing gas". American physician Crawford W. Long noticed that his friends felt no pain when they injured themselves while staggering around under the influence of diethyl ether.

He immediately thought of its potential in surgery. Conveniently, a participant in one of those "ether frolics", a student named James Venable, had two small tumors he wanted excised. But fearing the pain of surgery, Venable kept putting the operation off. Hence, Long suggested that he have his operation while under the influence of ether.

Venable agreed, and on 30 March he underwent a painless operation. However, Long did not announce his discovery until Horace Wells conducted the first public demonstration of the inhalational anesthetic at the Massachusetts General Hospital in Boston in However, the nitrous oxide was improperly administered and the patient cried out in pain. This occurred in the surgical amphitheater now called the Ether Dome. The previously skeptical Warren was impressed and stated, "Gentlemen, this is no humbug.

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Morton at first attempted to hide the actual nature of his anesthetic substance, referring to it as Letheon. He received a US patent for his substance, but news of the successful anesthetic spread quickly by late Respected surgeons in Europe including Liston , Dieffenbach , Pirogov , and Syme quickly undertook numerous operations with ether.

This was the first case of an operator-anesthetist. Scott used ether for a surgical procedure.

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Drawbacks with ether such as excessive vomiting and its explosive flammability led to its replacement in England with chloroform. In , Dr Robert Mortimer Glover in London discovered the anaesthetic qualities of chloroform on laboratory animals. This led to many deaths from the use of chloroform that with hindsight might have been preventable. The first fatality directly attributed to chloroform anesthesia was recorded on 28 January after the death of Hannah Greener. The first comprehensive medical textbook on the subject, Anesthesia , was authored in by anesthesiologist Dr.

James Tayloe Gwathmey and the chemist Dr. Of these first famous anesthetics, only nitrous oxide is still widely used today, with chloroform and ether having been replaced by safer but sometimes more expensive general anesthetics , and cocaine by more effective local anesthetics with less abuse potential. Almost all healthcare providers use anesthetic drugs to some degree, but most health professions have their own field of specialists in the field including medicine, nursing and dentistry. Doctors specializing in anaesthesiology , including perioperative care, development of an anesthetic plan, and the administration of anesthetics are known in the US as anesthesiologists and in the UK, Canada, Australia, and NZ as anaesthetists or anaesthesiologists.

Nurse anesthetists also administer anesthesia in nations. A word with surprisingly literal origins. Do you feel lucky? How we chose 'justice'. And is one way more correct than the others? How to use a word that literally drives some people nuts. The awkward case of 'his or her'. Identify the word pairs with a common ancestor. Can you spell these 10 commonly misspelled words?

Examples of anesthetize in a Sentence The doctor anesthetized the patient by an intravenous injection. She was anesthetized before the operation. Recent Examples on the Web Sodium thiopental, the barbiturate used in the injection that killed Brooks, and pancuronium bromide are typically used in medical settings to anesthetize patients — they were not designed for use in lethal injection procedures. Could it work for people? Film Review Cannes ," 15 May These example sentences are selected automatically from various online news sources to reflect current usage of the word 'anesthetize.

First Known Use of anesthetize , in the meaning defined above.