Classes of Neuroanesthesia: Comparison
View Latest Version
Please note this is a comparison between Version 2 by Wendy Huang and Version 1 by Brandon Lucke-Wold.

Anesthesia in neurosurgery embodies a vital element in the development of neurosurgical intervention. This undisputed interest has offered surgeons and anesthesiologists an array of anesthetic selections to utilize, though with this allowance comes the equally essential requirement of implementing a maximally appropriate agent. General anesthetic agents can be categorized as those administered intravenously or inhaled, both pairs granting unique advantages. The latter of which can be further subdivided into either volatile or non-volatile agents. As the methods of administration vary, so do the proposed mechanisms of action for these substances.

  • neuroanesthesia
  • total intravenous anesthesia
  • volatile anesthetics

1. Introduction

As neuroanesthetic induction and maintenance must balance the preservation of stable hemodynamics and perfusion of cerebral tissues with alterations to intracranial pressure that such perfusion may incur, it is pertinent to note the systemic effects of these various anesthetic agents in neurosurgical procedures [3][1]. This consideration not only ensures that the metabolic demands of the organs of the central nervous system are met, but also reduces injury and trauma to them. Most anesthetic agents, with the exception of ketamine, reduce the overall global oxygen metabolism of the brain, whereas the cerebral blood flow is increased by volatile anesthetics, nitrous oxide, and ketamine but reduced by other intravenous agents [3][1]. Such changes in physiological parameters impinge upon several endogenous mechanisms including cerebral autoregulation, vasomotor reactivity, and neurovascular coupling, of which anesthetic agents have varied effects [3][1].
Cerebral autoregulation entails adjustments to vascular tone that are sensitive to both long-term and short-term changes in systemic blood pressure [9][2]. These changes are hypothesized to be regulated myogenically or endothelially in response to stress on the vasculature, neurogenically by the autonomic nervous system and neurons, and to some extent metabolically [10][3]. Volatile anesthetic agents have been found to reduce cerebral autoregulation at higher doses, and propofol in particular has been found to reduce it at levels >200 mcg/kg/min [3][1]. In addition, synthetic opioids have been found to increase cerebral blood flow by vasodilation as a result of such cerebrovascular autoregulation [11][4]. The vasomotor reactivity of cerebral arterioles arises from pH changes to vasculature and surrounding smooth muscles, and as such, is largely dependent on the partial pressure of carbon dioxide: increases in PaCO2 have been shown to have vasodilatory effects, increasing blood flow [3][1]. The vasomotor reactivity is reduced at higher concentrations of certain volatile agents and has been shown to be variably affected by propofol [3][1]. Neurovascular coupling can be thought of as a combination of phasic and tonic vasomodulation regulated by the production of substances and metabolites by neurons and astrocytes, respectively. The role of these various anesthetic agents on neurovascular coupling has yet to be fully determined but they have been shown to affect neural activity as well as subsequent vasoactive signal transmission, and vasoactive response as well [3,12][1][5]. Most notably, etomidate, propofol, and barbiturates have been found to decrease cerebral blood flow secondary to decreased cerebral metabolic demands [3][1].
Intracranial pressure, determined by the pressure within the skull exerted by its content in the form of blood volume, tissue volume, and cerebrospinal fluid volume, is functionally related to cerebral perfusion pressure, and affected by overall cerebral blood flow [13][6]. As such, alterations in cerebral blood flow following the use of anesthetic agents subsequently coincide with changes in intracranial pressure, as demonstrated through the Cushing reflex equation:
 
CPP   =   MAP   −   ICP
where CPP is cerebral perfusion pressure, MAP is mean arterial pressure, and ICP is intracranial pressure [10][3].

2. Total Intravenous Anesthetics

The first mention of total intravenous anesthesia (TIVA) in the literature dates to 1872 in a report by Pierre-Cyprine describing the use of chloride hydrate [15][7]. Following the introduction of propofol in 1977, the archetypal TIVA, TIVA utilization rapidly increased [16][8]. Propofol increases GABA-mediated chloride channels in the brain resulting in inhibitory tone in the CNS. Furthermore, the drug increases the duration of the GABA’s effects by decreasing dissociation from its receptor, leading to the hyperpolarization of the cell membrane [17][9]. Its effects have a rapid onset and are short-acting, which allows for rapid recovery post-surgery and evaluation of neurological function [18][10]. Propofol also decreases intracranial pressure, cerebral blood flow, cerebral metabolism, and edema while supporting cerebral perfusion pressure and mean arterial pressure. This aggregate of effects is neuroprotective during cerebral ischemia [19][11]. Furthermore, the administration of propofol with an opioid provides hypnosis, amnesia, and minimizes response and movement to surgical stimulation, achieving all of the factors of a true anesthetic while also decreasing postoperative nausea and vomiting [16,18][8][10]. TIVA is now generally classified as the combined use of a hypnotic agent (e.g., propofol) and an opioid (e.g., fentanyl or remifentanil) without concurrent use of inhaled anesthetics [20,21][12][13]. Additionally, TIVA is conducive to new considerations that have emerged in neurosurgery anesthesia such as minimizing affected brain function and electrophysiological monitoring. Due to propofol’s rapid onset and short duration, infusion rates can be adjusted to allow for patient cooperation when necessary during a procedure [18][10]. Current common intravenous agents include thiopentone, propofol, etomidate, ketamine, benzodiazepines, and opioids [19][11].

3. Volatile Anesthetics

Diethyl ether was identified centuries ago and may have been originally compounded by an 8th-century Arabian philosopher. However, it was not until 1842 that the first use of ether for surgical anesthesia was documented [22][14]. More than 150 years after this discovery of a form of general anesthesia, volatile agents are still in clinical use today [23][15]. While the precise mechanism of action of volatile anesthetics remains largely unknown, studies have demonstrated that they are active in the central nervous system, augmenting GABA receptors and stimulating potassium channels [8][16]. Additionally, these agents have a role in depressing excitatory pathways including acetylcholine receptors, glutamate receptors, serotonin receptors, muscarinic receptors, and nicotinic receptors [8][16]. They are most often administered through a face mask, laryngeal mask, or endotracheal tube. While induction with volatile agents is often preferred in infants and young children because it allows for a needleless experience while awake, adult patients typically undergo an intravenous induction to reduce risks inherent to a full-grown patient. In a randomized double-blind comparison of 8% sevoflurane and propofol as anesthetic agents, Thwaites et al. found that induction with sevoflurane was associated with a lower rate of apnea, decreased time to establish spontaneous ventilation, and a smoother transition to maintenance. Furthermore, emergence was found to be earlier with sevoflurane [24][17]. While volatile agents have few absolute contraindications beyond gene variants for malignant hyperthermia, in the field of neurosurgery, these agents have concerns as they have been shown to decrease cerebral perfusion and increase intracerebral pressure [21,25][13][18]. Some of the most common volatile anesthetics in use today include halothane, isoflurane, desflurane, and sevoflurane.

4. Advantages and Disadvantages of Anesthetic Options

When administering anesthesia to neurosurgical patients, the onus is on the anesthetist to gauge whether inhaled or intravenous anesthetics would be more advantageous. Three of the most significant considerations regarding a neurosurgical anesthetic are the effects on hemodynamics, intracranial pressure, and postoperative conditions [19][11]. Hemodynamic stability is needed to maintain cerebral autoregulation [26][19]. Furthermore, the intrinsic autoregulation of factors (e.g., partial CO2 pressure and mean arterial pressure) that influence hemodynamic stability may be lost via the circumstances precipitating neurosurgical management [27,28][20][21]. Therefore, hemodynamic consideration is especially important within the context of neurosurgical anesthesia. In a randomized study, Strebel et al. demonstrated that volatile agents can impair autoregulation while propofol is helpful in preserving it [29][22]. Furthermore, Van Hemelrijck et al. demonstrated that the use of a propofol-loading infusion did not change the measure of blood pressure or heart rate, demonstrating the benefits of TIVA within the context of hemodynamics [30][23]. Low intracranial pressure is a significant factor allowing for optimal operating conditions and can also be neuroprotective. In a randomized prospective study, Petersen et al. found that subdural intracranial pressure was lower and cerebral perfusion pressure was higher in patients anesthetized by propofol compared to sevoflurane- or isoflurane-anesthetized patients [31][24]. This finding suggests that TIVA is beneficial in neurological surgery by minimizing local hypoperfusion and cerebral ischemia. Following surgery, rapid recovery from anesthesia is important to allow for neurological examination. Regarding the duration of effect, both TIVA with propofol-remifentanil and volatile agents have short half-lives, allowing for a rapid recovery after surgery [32][25]. This is supported in the literature as demonstrated by a randomized sample of patients undergoing craniotomy. Here, Talke et al. demonstrate that there was no difference between early post-operative recovery variables such as recovery time and early cognition [33][26]. An appraisal of the present literature of randomized-controlled trials comparing anesthetic agents head-to-head across various peri and postoperative parameters are included in Table 1 and Table 2 [30,31,32,33,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72][23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61][62][63][64].
Table 1.
Published trials of general anesthetic agents for cranial procedures.
Authors and Year Surgical Procedure Comparison Findings
Aken et al., 1990 [35][27] Unspecified cranial procedure Balanced anesthesia (loading thiopental and fentanyl + maintenance fentanyl, droperidol, thiopental, and isoflurane in nitrous oxide, n = 20) vs. TIVA (loading propofol + alfentanil infusion, n = 20) During induction, TIVA had a significantly greater hemodynamic stability. Balance anesthesia was associated with a significantly longer emergence time than TIVA.
Hemelrijck et al., 1991 [30][23] Craniotomy for resection of brain tumor Propofol (n = 20) vs. thiopental (n = 20) Postoperative return to orientation time was shorter in the propofol group (7 +/− 5 min vs. 27 +/− 23 min).
Ornstein et al., 1993 [36][28] Craniotomy for resection of supratentorial lesion Anesthetic maintenance via desflurane (n = 12) vs. isoflurane (n = 12) CBF values were non-significantly different as measured at 1 MAC and 1.5 MAC concentrations for both desflurane and isoflurane (p > 0.05), as well as at 1.25 MAC as measured in n = 15 patients (p > 0.05).
Talke et al., 1996 [37][29] Hypophysectomy Propofol (n = 10) vs. loading propofol + maintenance desflurane (n = 10) vs. loading propofol + maintenance isoflurane (n = 10) Minimum CPP was significantly lower in desflurane (p < 0.05) and isoflurane (p < 0.05) groups compared to propofol-only control. Minimum SBP was significantly lower in desflurane (p < 0.05) and isoflurane (p < 0.05) compared to propofol-only control.
Artru et al., 1997 [38][30] Unspecified cranial procedure Anesthetic maintenance via sevoflurane (n = 8) and isoflurane (n = 6) following induction via mannitol Neither sevoflurane or isoflurane significantly altered ICP, and both decreased middle cerebral artery flow velocity (Vmca). Notably, decreased Vmca with sevoflurane was related to decreased CPP at 0.5 MAC (p < 0.05), and increased CVRe at 1.0 and 1.5 MAC (p < 0.05). The CPP decreased from baseline at 0.5, 1.0, and 1.5 MACs of isoflurane (p < 0.05).
Hoffman et al., 1998 [39][31] Craniotomy for unspecified pathology Thiopental induction (n = 10) vs. desflurane (n = 10) Neither thiopental nor desflurane changed tissue gases or pH, but desflurane increased PO2 70% (p < 0.05), whereas thiopental decreased PO2 30% during temporary brain artery occlusion.
Talke et al., 1999 [40][32] Transsphenoidal Hypophysectomy Anesthetic maintenance via propofol (n = 10) vs. sevoflurane (n = 20) Sevoflurane increased lumbar CSF pressure and decreased CPP and systolic blood pressure following infusion while propofol did not affect lumbar CSF pressure, CPP, nor systolic blood pressure.
Talke et al., 2002 [33][26] Craniotomy for resection of supratentorial lesion Propofol (n = 20) vs. isoflurane (n = 20) Emergence time to eyes opening was not different between anesthetic agents (p > 0.05). There was no difference in occurrence of hypertension (p > 0.05).
Iwata et al., 2003 [41][33] Unspecified intracranial surgery Propofol (n = 13) vs. sevoflurane (n = 13) There was no difference in the rate of temperature decrease and recovery in induced hypothermia (p < 0.05).
Fraga et al., 2003 [42][34] Craniotomy for resection of supratentorial lesion Inhalation of isoflurane (n = 30) vs. desflurane (n = 30) following induction via fentanyl, thiopental, and vecuronium maintained with 60% nitrous oxide in oxygen There were no significant differences between MAP, ICP, and CPP between use of desflurane and isoflurane, but notable decreases (p < 0.05) in both groups from baseline values with regard to MAP and CPP. The ratio between the cerebral metabolic oxygen requirement and cerebral blood flow decreased significantly for both groups as well.
Petersen et al., 2003 [31][24] Craniotomy for resection of supratentorial tumor Propofol (n = 41) vs. isoflurane (n = 38) vs. sevoflurane (n = 38) No differences in ICP or CPP between anesthetic agents (p > 0.05).
Günes et al., 2005 [43][35] Unspecified intracranial procedure Anesthetic maintenance via propofol (n = 39) vs. dexmedetomidine (n = 39) Systolic blood pressure and MAP were not different between the two agents. Extubation time was shorter for propofol (p < 0.05). Analgesic requirements were higher for propofol (p = 0.013).
Magni et al., 2005 [32][25] Supratentorial craniotomy for unspecified pathology Propofol (n = 64) vs. sevoflurane (n = 64) Emergence time was not different between anesthetic agents. Occurrence of hypertension was higher in propofol than sevoflurane use (p = 0.0046), and hypotension was higher in propofol than sevoflurane (p = 0.02).
Sekimoto et al., 2006 [44][36] Craniotomy for resection of brain tumor Anesthetic maintenance via halothane vs. isoflurane vs. sevoflurane after induction via propofol/fentanyl/nitrous oxide Halothane, isoflurane, and sevoflurane were all found to reduce systolic blood pressure, but only sevoflurane and isoflurane decreased train-of-four ratios significantly at 1.0 MAC (p < 0.001). Amplitudes of transcranial motor-evoked potentials were reduced by isoflurane and sevoflurane at 0.5 MACs, but not halothane, reflecting the reduced extent of the neuromuscular blockade initiated by halothane.
Djian et al., 2006 [45][37] Unspecified intracranial procedure Remifentanil vs. sufentanil in combination with propofol for maintenance of anesthesia Remifentanil was associated with the need for less adjustments with regard to hemodynamic stability (p = 0.037), greater use of morphine (p = 0.01), and higher intraoperative opioid costs. However, there was no significant differences in extubation times between groups.
Bhagat et al., 2008 [46][38] Craniotomy for unspecified pathology Anesthetic maintenance via propofol (n = 50) vs. isoflurane (n = 50) Hypertension occurrence and MAP change were not different between the two agents. Emergence time was higher for propofol (p = 0.008).
Bonhomme et al., 2009 [47][39] Unspecified intracranial procedure Propofol (n = 30) vs. sevoflurane (n = 31) Propofol was associated with higher occurrence of intraoperative hypertension (p < 0.001) and sevoflurane was associated with higher occurrence of intraoperative hypotension (p = 0.015).
Ali et al., 2009 [48][40] Resection of pituitary tumor Propofol (n = 30), isoflurane (n = 30), sevoflurane (n = 30) Emergence time was significantly longer with use of isoflurane (p < 0.001). Hypertension occurrence was higher in isoflurane than in propofol or sevoflurane, and higher in sevoflurane than propofol (p < 0.001). Hypotension was not difference between anesthetics (p = 0.36).
Bilotta et al., 2009 [49][41] Craniotomy for resection of supratentorial lesion Sevoflurane (n = 28) vs. desflurane (n = 28) Significant delays in cognitive “awakening” for obese and overweight patients receiving sevoflurane-based anesthesia as compared to those receiving desflurane-based anesthesia as measured by post-operative short orientation memory concentration test scores at 15 and 30 min (p < 0.005, p < 0.005) as well as with the Rancho Los Amigos scale (p < 0.005)
Güneş et al., 2009 [71][63] Craniotomy for resection of supratentorial lesion Anesthetic maintenance with dexmedetomidine in addition to sevoflurane (n = 30), desflurane (n = 30), and isoflurane (n = 30) MAP was elevated following intubation for all groups. Rates of eyes opening and responsiveness following verbal commands were lower in desflurane–dexmedetomidine than in other groups (p = 0.001).
Magni et al., 2009 [72][64] Craniotomy for resection of supratentorial lesion Anesthetic maintenance via sevoflurane (n = 60) vs. desflurane (n = 60) Mean emergence was similar between the two groups, but extubation and recovery time were lower (p < 0.001) in the desflurane group. Hemodynamic stability differences were non-significant between the two groups.
Lauta et al., 2010 [50][42] Craniotomy for resection of supratentorial lesion Anesthetic maintenance via propofol (n = 153) vs. sevoflurane (n = 149) Propofol was associated with a significantly longer emergence time to eyes opening (p < 0.014. Sevoflurane was associated with higher occurrence of hypotension (p < 0.0167).
Yildiz et al., 2011 [51][43] Craniotomy for resection of supratentorial lesion Anesthetic maintenance via desflurane (n = 35) vs. isoflurane (n = 35) Heart rate was not different between the two agents. MAP was higher for desflurane (p < 0.05). Extubation time and eyes opening time was shorter for desflurane (p < 0.05).
Ghoneim et al., 2015 [52][44] Craniotomy for resection of supratentorial tumors Anesthetic maintenance via isoflurane (n = 20) vs. sevoflurane (n = 20) vs. desflurane (n = 20) Emergence times were significantly shorter for desflurane or sevoflurane than with isoflurane in pediatric patients following a craniotomy for supratentorial tumors.
Hernandez et al., 2015 [53][45] Craniotomy for hematoma Anesthetic maintenance via propofol (n = 20) or sevoflurane (n = 20) SSEPs amplitudes and latencies were not different between the two agents. TceMEPs amplitudes were higher for propofol (p < 0.05). Latencies were shorter in the propofol group (p < 0.05).
Goettel et al., 2016 [54][46] Awake craniotomy for unspecified pathology Dexmedetomidine (n = 25) vs. propofol (n = 25) There were no differences in level of sedation (OAA) (p = 0.13). There were no differences in intraoperative hypertension (p = 0.60), hypotension (p = 0.50), or complications (p = 0.99). There was no difference in postoperative complications (p > 0.05).
Gokcek et al., 2016 [55][47] Unspecified intracranial procedure Anesthetic maintenance via sevoflurane (n = 25) vs. desflurane (n = 25) Emergence time and time to eyes opening were higher with sevoflurane (p < 0.001).
Lin et al., 2016 [56][48] Resection of supratentorial lesion Anesthetic maintenance via propofol (n = 31) vs. dexmedetomidine (n = 31) NIHSS-positive change was higher in propofol than dexmedetomidine (p < 0.001). Focal neurologic deficits were higher in propofol than dexmedetomidine (p < 0.05).
Rajan et al., 2016 [57][49] Craniotomy or transsphenoidal approach for resection of brain tumor Dexmedetomidine (n = 68) vs. remifentanil (n = 71) Dexmedetomidine was associated with significantly lower postoperative MAP (p < 0.001). Dexmedetomidine was associated with significantly longer emergence time to open eyes (p < 0.001).
Thongrong et al., 2017 [58][50] Craniotomy for unspecified pathology Anesthetic maintenance via fentanyl (n = 30) vs. dexmedetomidine (n = 30) after propofol induction Dexmedetomidine infusions reduced adverse effects, with signs of effectively controlled systolic blood pressure one minute prior to skull pin insertion (p < 0.05), as well as during skull pin insertion (p < 0.01) in comparison to fentanyl. Similarly, dexmedetomidine infusions were related to reduced adverse hypertensive and hypotensive responses in patients.
Bhardwaj et al., 2018 [59][51] Surgical clipping for aneurysmal subarachnoid hemorrhage Propofol (n = 35) vs. desflurane (n = 35) There was no difference in blood loss (p < 0.05), hypotension (p < 0.05), hypertension (p < 0.05), or emergence time for eyes opening (p < 0.05).
Gracia et al., 2018 [60][52] Unspecified intracranial procedure Anesthetic induction via propofol (n = 20) vs. thiopental (n = 20) There was no difference in heart rate (p > 0.05). MAP was significantly higher in thiopental groups (p < 0.05). Systolic and diastolic blood pressure was significantly lower in thiopental groups (p < 0.05).
Molina et al., 2018 [61][53] Craniotomy for resection of tumor Propofol–remifentanil (n = 105) for asleep sedation vs. conscious sedation with dexmedetomidine (n = 75) Patients sedated with dexmedetomidine used less opiates, antihypertensive drugs, and had a lower postoperative duration and length of stay (all p < 0.001).
Xinyan et al., 2018 [62][54] Awake craniotomy for unspecified pathology Dexmedetomidine (n = 20), propofol (n = 20), etomidate (n = 20) There was no significant difference in perioperative wake up duration (p > 0.05) and postoperative emergence time (p > 0.05). The rate of adverse events was lower in dexmedetomidine than propofol and etomidate (p < 0.05). The rate of adverse events was lower in propofol than etomidate (p < 0.05).
Khallaf et al., 2019 [63][55] Craniotomy for hematoma Anesthetic maintenance via propofol (n = 20) vs. dexmedetomidine (n = 20) Tachycardia, bradycardia, and hypertension occurrences were not different between the two agents. IPP and CPP changes were not different between the two agents. Hypotension occurrences were higher in the propofol group (p = 0.024).
Preethi et al., 2021 [64][56] Craniotomy for hematoma Anesthetic maintenance via propofol (n = 45) vs. isoflurane Change in heart rate, systolic blood pressure, diastolic blood pressure, and MAP were not different between the two agents. Brain relaxation was higher for propofol (p < 0.05). ICP was higher for isoflurane (p = 0.01).
Balasubramanian et al., 2021 [65][57] Surgical clipping/endovascular coiling for aneurysmal subarachnoid hemorrhage Propofol (n = 8) vs. isoflurane (n = 8) vs. sevoflurane (n = 8), vs. desflurane (n = 8) There was no significant difference found between anesthetic on levels of CSF caspase-3 levels.
Table 2.
Published trials of general anesthetic agents for spinal procedures.
Authors and Year Surgical Procedure Comparison Findings
Laureau et al., 1999 [66][58] Posterior instrumentation for treatment of idiopathic scoliosis Induction via intravenous propofol (n = 15) vs. midazolam (n = 15) Cortical somatosensory-evoked potentials did not deteriorate in either the propofol or the midazolam induction groups.
Inoue et al., 2005 [67][59] Cervical spine surgery for unspecified pathology Anesthetic maintenance via fentanyl and propofol (n = 25) vs. fentanyl and <1% sevoflurane (n = 25) vs. sevoflurane (n = 25) Perception of pain and bucking scores following emergence- were greater for patients exposed to sevoflurane versus propofol and fentanyl and fentanyl and sevoflurane in combination.
Kurt et al., 2005 [68][60] Unspecified spinal procedure Anesthetic maintenance via isoflurane (n = 12) vs. sevoflurane (n = 10) vs. desflurane (n = 10) Sevoflurane and isoflurane administered via volatile anesthetics were able to achieve controlled hypotension in comparison to desflurane with systolic blood pressures outside the target range of 32% and 26% for isoflurane and sevoflurane, respectively, and 44% with desflurane.
Albertin et al., 2008 [69][61] Lumbar spine surgery for unspecified pathology Induction via sevoflurane (n = 14) or propofol (n = 14) as main anesthetic agents Peripheral blood flow was greater in the propofol group before and during the hypotensive period, but had reduced blood loss and intra-operative bleeding as compared to the sevoflurane group (p < 0.005).
Turgut et al., 2008 [70][62] Lumbar laminectomy Pre-operative bolus and anesthetic maintenance via dexmedetomidine (n = 25) vs. fentanyl (n = 25) following induction via propofol as well as maintenance Extubation and discharge times were similar between dexmedetomidine and fentanyl, but MAP values after intubation for those exposed to dexmedetomidine were higher for those exposed to fentanyl before and after extubation. Supplemental analgesia was required earlier for fentanyl group patients (34.8 +/− 1.35 min vs. 60.4 +/− 1.04 min).

References

  1. Slupe, A.M.; Kirsch, J.R. Effects of anesthesia on cerebral blood flow, metabolism, and neuroprotection. J. Cereb. Blood Flow. Metab. 2018, 38, 2192–2208.
  2. Silverman, A.; Petersen, N.H. Physiology, Cerebral Autoregulation. In StatPearls; StatsPearls Publishing: Treasure Island, FL, USA, 2022.
  3. Armstead, W.M. Cerebral Blood Flow Autoregulation and Dysautoregulation. Anesthesiol. Clin. 2016, 34, 465–477.
  4. Bazin, J.E. Effects of anesthetic agents on intracranial pressure. Ann. Fr. Anesth. Reanim. 1997, 16, 445–452.
  5. Masamoto, K.; Kanno, I. Anesthesia and the quantitative evaluation of neurovascular coupling. J. Cereb. Blood Flow. Metab. 2012, 32, 1233–1247.
  6. Tomas Partington, A.F. Intracranial pressure and cerebral blood flow. Anaesth. Intensive Care Med. 2014, 15, 189–194.
  7. Searles, P.W. Intravenous Anesthesia. JAMA 1942, 118, 117–119.
  8. Kay, B.; Rolly, G.I.C.I. 35868, a new intravenous induction agent. Acta Anaesthesiol. Belg. 1977, 28, 303–316.
  9. Antkowiak, B.; Rammes, G. GABA(A) receptor-targeted drug development -New perspectives in perioperative anesthesia. Expert Opin. Drug Discov. 2019, 14, 683–699.
  10. Hans, P.; Bonhomme, V. Why we still use intravenous drugs as the basic regimen for neurosurgical anaesthesia. Curr. Opin. Anaesthesiol. 2006, 19, 498–503.
  11. Cole, C.D.; Gottfried, O.N.; Gupta, D.K.; Couldwell, W.T. Total intravenous anesthesia: Advantages for intracranial surgery. Neurosurgery 2007, 61, 369–377; discussion 377–368.
  12. Dershwitz, M.; Michalowski, P.; Chang, Y.; Rosow, C.E.; Conlay, L.A. Postoperative nausea and vomiting after total intravenous anesthesia with propofol and remifentanil or alfentanil: How important is the opioid? J. Clin. Anesth. 2002, 14, 275–278.
  13. Demirbilek, S.; Ganidagli, S.; Aksoy, N.; Becerik, C.; Baysal, Z. The effects of remifentanil and alfentanil-based total intravenous anesthesia (TIVA) on the endocrine response to abdominal hysterectomy. J. Clin. Anesth. 2004, 16, 358–363.
  14. Whalen, F.X.; Bacon, D.R.; Smith, H.M. Inhaled anesthetics: An historical overview. Best Pract. Res. Clin. Anaesthesiol. 2005, 19, 323–330.
  15. Gaya da Costa, M.; Kalmar, A.F.; Struys, M. Inhaled Anesthetics: Environmental Role, Occupational Risk, and Clinical Use. J. Clin. Med. 2021, 10, 1306.
  16. Deng, J.; Lei, C.; Chen, Y.; Fang, Z.; Yang, Q.; Zhang, H.; Cai, M.; Shi, L.; Dong, H.; Xiong, L. Neuroprotective gases—Fantasy or reality for clinical use? Prog. Neurobiol. 2014, 115, 210–245.
  17. Thwaites, A.; Edmends, S.; Smith, I. Inhalation induction with sevoflurane: A double-blind comparison with propofol. Br. J. Anaesth. 1997, 78, 356–361.
  18. Ergun, R.; Akdemir, G.; Sen, S.; Tasci, A.; Ergungor, F. Neuroprotective effects of propofol following global cerebral ischemia in rats. Neurosurg. Rev. 2002, 25, 95–98.
  19. Paulson, O.B.; Strandgaard, S.; Edvinsson, L. Cerebral autoregulation. Cerebrovasc. Brain Metab. Rev. 1990, 2, 161–192.
  20. Dagal, A.; Lam, A.M. Cerebral autoregulation and anesthesia. Curr. Opin. Anaesthesiol. 2009, 22, 547–552.
  21. Hughey, A.B.; Lesniak, M.S.; Ansari, S.A.; Roth, S. What will anesthesiologists be anesthetizing? Trends in neurosurgical procedure usage. Anesth. Analg. 2010, 110, 1686–1697.
  22. Strebel, S.; Lam, A.M.; Matta, B.; Mayberg, T.S.; Aaslid, R.; Newell, D.W. Dynamic and static cerebral autoregulation during isoflurane, desflurane, and propofol anesthesia. Anesthesiology 1995, 83, 66–76.
  23. Van Hemelrijck, J.; Van Aken, H.; Merckx, L.; Mulier, J. Anesthesia for craniotomy: Total intravenous anesthesia with propofol and alfentanil compared to anesthesia with thiopental sodium, isoflurane, fentanyl, and nitrous oxide. J. Clin. Anesth. 1991, 3, 131–136.
  24. Petersen, K.D.; Landsfeldt, U.; Cold, G.E.; Petersen, C.B.; Mau, S.; Hauerberg, J.; Holst, P.; Olsen, K.S. Intracranial pressure and cerebral hemodynamic in patients with cerebral tumors: A randomized prospective study of patients subjected to craniotomy in propofol-fentanyl, isoflurane-fentanyl, or sevoflurane-fentanyl anesthesia. Anesthesiology 2003, 98, 329–336.
  25. Magni, G.; Baisi, F.; La Rosa, I.; Imperiale, C.; Fabbrini, V.; Pennacchiotti, M.L.; Rosa, G. No difference in emergence time and early cognitive function between sevoflurane-fentanyl and propofol-remifentanil in patients undergoing craniotomy for supratentorial intracranial surgery. J. Neurosurg. Anesthesiol. 2005, 17, 134–138.
  26. Talke, P.; Caldwell, J.E.; Brown, R.; Dodson, B.; Howley, J.; Richardson, C.A. A comparison of three anesthetic techniques in patients undergoing craniotomy for supratentorial intracranial surgery. Anesth. Analg. 2002, 95, 430–435.
  27. Van Aken, H.; Van Hemelrijck, J.; Merckx, L.; Mollhoff, T.; Mulier, J.; Lubbesmeyer, H.J. Total intravenous anesthesia using propofol and alfentanil in comparison with balanced anesthesia in neurosurgery. Anasth Intensiv. Notf. 1990, 25, 54–58.
  28. Ornstein, E.; Young, W.L.; Fleischer, L.H.; Ostapkovich, N. Desflurane and isoflurane have similar effects on cerebral blood flow in patients with intracranial mass lesions. Anesthesiology 1993, 79, 498–502.
  29. Talke, P.; Caldwell, J.; Dodsont, B.; Richardson, C.A. Desflurane and isoflurane increase lumbar cerebrospinal fluid pressure in normocapnic patients undergoing transsphenoidal hypophysectomy. Anesthesiology 1996, 85, 999–1004.
  30. Artru, A.A.; Lam, A.M.; Johnson, J.O.; Sperry, R.J. Intracranial pressure, middle cerebral artery flow velocity, and plasma inorganic fluoride concentrations in neurosurgical patients receiving sevoflurane or isoflurane. Anesth. Analg. 1997, 85, 587–592.
  31. Hoffman, W.E.; Charbel, F.T.; Edelman, G.; Ausman, J.I. Thiopental and desflurane treatment for brain protection. Neurosurgery 1998, 43, 1050–1053.
  32. Talke, P.; Caldwell, J.E.; Richardson, C.A. Sevoflurane increases lumbar cerebrospinal fluid pressure in normocapnic patients undergoing transsphenoidal hypophysectomy. Anesthesiology 1999, 91, 127–130.
  33. Iwata, T.; Inoue, S.; Kawaguchi, M.; Takahashi, M.; Sakamoto, T.; Kitaguchi, K.; Furuya, H.; Sakaki, T. Comparison of the effects of sevoflurane and propofol on cooling and rewarming during deliberate mild hypothermia for neurosurgery. Br. J. Anaesth. 2003, 90, 32–38.
  34. Fraga, M.; Rama-Maceiras, P.; Rodino, S.; Aymerich, H.; Pose, P.; Belda, J. The effects of isoflurane and desflurane on intracranial pressure, cerebral perfusion pressure, and cerebral arteriovenous oxygen content difference in normocapnic patients with supratentorial brain tumors. Anesthesiology 2003, 98, 1085–1090.
  35. Günes, Y.; Gündüz, M.; Özcengiz, D.; Özbek, H.; Isik, G. Dexmedetomidine-Remifentanil or Propofol-Remifentanil Anesthesia in Patients Undergoing Intracranial Surgery. Neurosurg. Q. 2005, 15, 122–126.
  36. Sekimoto, K.; Nishikawa, K.; Ishizeki, J.; Kubo, K.; Saito, S.; Goto, F. The effects of volatile anesthetics on intraoperative monitoring of myogenic motor-evoked potentials to transcranial electrical stimulation and on partial neuromuscular blockade during propofol/fentanyl/nitrous oxide anesthesia in humans. J. Neurosurg. Anesthesiol. 2006, 18, 106–111.
  37. Djian, M.C.; Blanchet, B.; Pesce, F.; Sermet, A.; Disdet, M.; Vazquez, V.; Gury, C.; Roux, F.X.; Raggueneau, J.L.; Coste, J.; et al. Comparison of the time to extubation after use of remifentanil or sufentanil in combination with propofol as anesthesia in adults undergoing nonemergency intracranial surgery: A prospective, randomized, double-blind trial. Clin. Ther. 2006, 28, 560–568.
  38. Bhagat, H.; Dash, H.H.; Bithal, P.K.; Chouhan, R.S.; Pandia, M.P. Planning for early emergence in neurosurgical patients: A randomized prospective trial of low-dose anesthetics. Anesth. Analg. 2008, 107, 1348–1355.
  39. Bonhomme, V.; Demoitie, J.; Schaub, I.; Hans, P. Acid-base status and hemodynamic stability during propofol and sevoflurane-based anesthesia in patients undergoing uncomplicated intracranial surgery. J. Neurosurg. Anesthesiol. 2009, 21, 112–119.
  40. Ali, Z.; Prabhakar, H.; Bithal, P.K.; Dash, H.H. Bispectral index-guided administration of anesthesia for transsphenoidal resection of pituitary tumors: A comparison of 3 anesthetic techniques. J. Neurosurg. Anesthesiol. 2009, 21, 10–15.
  41. Bilotta, F.; Doronzio, A.; Cuzzone, V.; Caramia, R.; Rosa, G.; Group, P.S. Early postoperative cognitive recovery and gas exchange patterns after balanced anesthesia with sevoflurane or desflurane in overweight and obese patients undergoing craniotomy: A prospective randomized trial. J. Neurosurg. Anesthesiol. 2009, 21, 207–213.
  42. Lauta, E.; Abbinante, C.; Del Gaudio, A.; Aloj, F.; Fanelli, M.; de Vivo, P.; Tommasino, C.; Fiore, T. Emergence times are similar with sevoflurane and total intravenous anesthesia: Results of a multicenter RCT of patients scheduled for elective supratentorial craniotomy. J. Neurosurg. Anesthesiol. 2010, 22, 110–118.
  43. Yildiz, K.; Bicer, C.; Aksu, R.; Dogru, K.; Madenoglu, H.; Boyaci, A. A comparison of 1 minimum alveolar concentration desflurane and 1 minimum alveolar concentration isoflurane anesthesia in patients undergoing craniotomy for supratentorial lesions. Curr. Ther. Res. Clin. Exp. 2011, 72, 49–59.
  44. Ghoneim, A.A.; Azer, M.S.; Ghobrial, H.Z.; El Beltagy, M.A. Awakening properties of isoflurane, sevoflurane, and desflurane in pediatric patients after craniotomy for supratentorial tumours. J. Neurosurg. Anesthesiol. 2015, 27, 1–6.
  45. Hernandez-Palazon, J.; Fuentes-Garcia, D.; Domenech-Asensi, P.; Piqueras-Perez, C.; Falcon-Arana, L.; Burguillos-Lopez, S. A comparison of equivolume, equiosmolar solutions of hypertonic saline and mannitol for brain relaxation during elective supratentorial craniotomy. Br. J. Neurosurg. 2016, 30, 70–75.
  46. Goettel, N.; Bharadwaj, S.; Venkatraghavan, L.; Mehta, J.; Bernstein, M.; Manninen, P.H. Dexmedetomidine vs propofol-remifentanil conscious sedation for awake craniotomy: A prospective randomized controlled trial. Br. J. Anaesth. 2016, 116, 811–821.
  47. Gokcek, E.; Kaydu, A.; Akdemir, M.S.; Akil, F.; Akinci, I.O. Early postoperative recovery after intracranial surgical procedures. Comparison of the effects of sevoflurane and desflurane. Acta Cir. Bras. 2016, 31, 638–644.
  48. Lin, N.; Han, R.; Zhou, J.; Gelb, A.W. Mild Sedation Exacerbates or Unmasks Focal Neurologic Dysfunction in Neurosurgical Patients with Supratentorial Brain Mass Lesions in a Drug-specific Manner. Anesthesiology 2016, 124, 598–607.
  49. Rajan, S.; Hutcherson, M.T.; Sessler, D.I.; Kurz, A.; Yang, D.; Ghobrial, M.; Liu, J.; Avitsian, R. The Effects of Dexmedetomidine and Remifentanil on Hemodynamic Stability and Analgesic Requirement After Craniotomy: A Randomized Controlled Trial. J Neurosurg. Anesthesiol. 2016, 28, 282–290.
  50. Thongrong, C.; Sirikannarat, P.; Kasemsiri, P.; Duangthongphon, P. Comparison of dexmedetomidine and fentanyl to prevent haemodynamic response to skull pin application in neurosurgery: Double blind randomized controlled trial. Anaesthesiol. Intensive Ther. 2017, 49, 268–273.
  51. Bhardwaj, A.; Bhagat, H.; Grover, V.K.; Panda, N.B.; Jangra, K.; Sahu, S.; Singla, N. Comparison of propofol and desflurane for postanaesthetic morbidity in patients undergoing surgery for aneurysmal SAH: A randomized clinical trial. J. Anesth. 2018, 32, 250–258.
  52. Gracia, C.Z.; Hanafie, A.; Nasution, A.H. Comparison of hemodynamic response between propofol and thiopental as an induction agent in neurosurgery anesthesia at Haji Adam Malik General Hospital Medan-Indonesa. Bali Med. J. 2018, 7, 712–722.
  53. Suero Molina, E.; Schipmann, S.; Mueller, I.; Wolfer, J.; Ewelt, C.; Maas, M.; Brokinkel, B.; Stummer, W. Conscious sedation with dexmedetomidine compared with asleep-awake-asleep craniotomies in glioma surgery: An analysis of 180 patients. J. Neurosurg. 2018, 129, 1223–1230.
  54. Xinyan, Z.; Xuekang, Z.; Sisi, L.; Xinhua, F.; Shi, S.; Zhiyi, L. Effects of dexmedetomidine, propofol and etomidate on the intraoperative wake-up in the cerebral functional area under the guidance of entropy index. Pharmazie 2018, 73, 647–650.
  55. Khallaf, M.; Thabet, A.M.; Ali, M.; Sharkawy, E.; Abdel-rehim, S. The effect of dexmedetomidine versus propofol in traumatic brain injury: Evaluation of some hemodynamic and intracranial pressure changes. Egypt. J. Neurosurg. 2019, 34, 17.
  56. Preethi, J.; Bidkar, P.U.; Cherian, A.; Dey, A.; Srinivasan, S.; Adinarayanan, S.; Ramesh, A.S. Comparison of total intravenous anesthesia vs. inhalational anesthesia on brain relaxation, intracranial pressure, and hemodynamics in patients with acute subdural hematoma undergoing emergency craniotomy: A randomized control trial. Eur. J. Trauma Emerg. Surg. 2021, 47, 831–837.
  57. Balasubramanian, M.; Kuberan, A.; Rawat, A.; Dhandapani, S.; Panda, N.; Kumar, A.; Sahoo, A.K.; Kumar, M.; Sharma, T.; Garcia, P.S.; et al. Effect of General Anesthetics on Caspase-3 Levels in Patients With Aneurysmal Subarachnoid Hemorrhage: A Preliminary Study. J. Neurosurg. Anesthesiol. 2021, 33, 172–176.
  58. Laureau, E.; Marciniak, B.; Hebrard, A.; Herbaux, B.; Guieu, J.D. Comparative study of propofol and midazolam effects on somatosensory evoked potentials during surgical treatment of scoliosis. Neurosurgery 1999, 45, 69–74.
  59. Inoue, Y.; Koga, K.; Sata, T.; Shigematsu, A. Effects of fentanyl on emergence characteristics from anesthesia in adult cervical spine surgery: A comparison of fentanyl-based and sevoflurane-based anesthesia. J. Anesth. 2005, 19, 12–16.
  60. Kurt, F.; Derbent, A.; Demirag, K.; Eris, O.; Uyar, M.; Islekel, S. Old method, new drugs: Comparison of the efficacy of sevoflurane, isoflurane, and desflurane in achieving controlled hypotension in spinal surgery. Adv. Ther. 2005, 22, 234–240.
  61. Albertin, A.; La Colla, L.; Gandolfi, A.; Colnaghi, E.; Mandelli, D.; Gioia, G.; Fraschini, G. Greater peripheral blood flow but less bleeding with propofol versus sevoflurane during spine surgery: A possible physiologic model? Spine 2008, 33, 2017–2022.
  62. Turgut, N.; Turkmen, A.; Gokkaya, S.; Altan, A.; Hatiboglu, M.A. Dexmedetomidine-based versus fentanyl-based total intravenous anesthesia for lumbar laminectomy. Minerva Anestesiol. 2008, 74, 469–474.
  63. Güneş, Y.; Türktan, M.; Erman, T.; Özbek, H.; Işik, G. Anesthesia for craniotomy: Comparison of sevoflurane, desflurane, or isoflurane anesthesia supplemented with an infusion of dexmedetomidine during supratentorial craniotomy. Neurosurg. Q. 2009, 19, 110–115.
  64. Magni, G.; La Rosa, I.; Melillo, G.; Savio, A. and Rosa, G. A comparison between sevoflurane and desflurane anesthesia in patients undergoing craniotomy for supratentorial intracranial surgery. Anesth Analg. 2009, 109, 567–571.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/)
Video Production Service
Feedback