Awake craniotomy using dexmedetomidine and scalp blocks: a retrospective cohort study

  • Niamh McAuliffeEmail author
  • Stuart Nicholson
  • Andrea Rigamonti
  • Gregory M. T. Hare
  • Michael Cusimano
  • Marco Garavaglia
  • Iryna Pshonyak
  • Sunit Das
Reports of Original Investigations



Anesthetic and surgical considerations for awake craniotomy (AC) include airway patency, patient comfort, and optimization of real-time brain mapping. The purpose of this study is to report our experience of using dexmedetomidine and scalp blocks, without airway intervention, as a means to facilitate and optimize intraoperative brain mapping and brain tumour resection during AC.


We conducted a retrospective cohort study of 55 patients who underwent AC from March 2012 to September 2016. The incidence of critical airway outcomes, perioperative complications, and successful intraoperative mapping was determined. The primary outcome was the incidence of a failed AC anesthetic technique as defined by the need to convert to general anesthesia with a secured airway prior to (or during) brain mapping and brain tumour resection. Secondary outcomes were the intraoperative incidence of: 1) altered surgical management due to information acquired through real-time brain mapping, 2) interventions to restore airway patency or rescue the airway, 3) hemodynamic instability (> 20% from baseline), 4) nausea and vomiting, 5) new onset neurologic deficits, and 6) seizure activity.


There were no anesthesia-related critical events and no patients required airway manipulation or conversion to a general anesthetic. Multimodal language, motor, and sensory assessment with direct cortical electrical stimulation was successfully performed in 100% of cases. In 24% (13/55) of patients, data acquired during intraoperative brain mapping influenced surgical decision-making regarding the extent of tumour resection. Nine (16%) patients had intraoperative seizures.


Dexmedetomidine-based anesthesia and scalp block facilitated AC surgery without any requirement for urgent airway intervention or unplanned conversion to a full general anesthetic. This approach can enable physiologic testing before and during tumour resection facilitating real-time surgical decision-making based on intraoperative brain mapping with patients awake thereby minimizing the risk of neurologic deficit and increasing the opportunity for optimal surgical resection.

Craniotomie sur patient éveillé utilisant la dexmédétomidine et des blocs des nerfs du scalp: une étude de cohorte rétrospective



Les considérations anesthésiques et chirurgicales faisant envisager une craniotomie sur patient éveillé (CE) sont notamment la perméabilité des voies aériennes, le confort du patient et l’optimisation de la cartographie cérébrale en temps réel. L’objectif de cette étude est de rapporter notre expérience de l’utilisation de la dexmédétomidine et des blocs des nerfs du scalp, sans intervention sur les voies aériennes, afin de faciliter et d’optimiser la cartographie cérébrale peropératoire et la résection de tumeurs cérébrales au cours d’une CE.


Nous avons mené une étude de cohorte rétrospective sur 55 patients ayant subi une CE entre mars 2012 et septembre 2016. L’incidence des événements critiques sur les voies aériennes, des complications périopératoires et des succès de la cartographie cérébrale peropératoire a été déterminée. Le critère d’évaluation principal était l’incidence de l’échec de la technique anesthésique par CE, défini par la nécessité de la convertir en anesthésie générale avec sécurisation des voies aériennes avant (ou pendant) la cartographie cérébrale et la résection de la tumeur. Les critères d’évaluation secondaires étaient des mesures de la survenue peropératoire des événements suivants : 1) modification de la gestion chirurgicale en raison d’informations acquises au cours de la cartographie cérébrale en temps réel, 2) interventions visant à restaurer la perméabilité des voies aériennes ou libérer l’accès aux voies aériennes, 3) instabilité hémodynamique (> 20 % par rapport à l’inclusion), 4) nausées et vomissements, 5) apparition de nouveaux déficits neurologiques, et 6) convulsion.


Il n’y a pas eu d’événements critiques liés à l’anesthésie et aucun patient n’a nécessité d’intervention sur les voies aériennes ou de conversion à une anesthésie générale. Une évaluation multimodale du langage, de la motricité et de la sensibilité avec stimulation électrique corticale a été réalisée avec succès dans 100 % des cas. Chez 24 % des patients (13/55), les données acquises au cours de la cartographie cérébrale peropératoire ont influencé la prise de décision concernant l’étendue de la résection tumorale. Neuf patients (16 %) ont présenté des convulsions peropératoires.


L’anesthésie basée sur la dexmédétomidine et le bloc des nerfs du scalp a facilité l’intervention de CE sans nécessiter aucune intervention urgente sur les voies aériennes ou conversion non prévue en anesthésie généralisée complète. Cette approche autorise la réalisation de tests physiologiques avant et pendant la résection de la tumeur, facilitant la prise de décision chirurgicale en temps réel basée sur la cartographie cérébrale peropératoire chez des patients éveillés, minimisant ainsi le risque de déficit neurologique et augmentant les chances de résection chirurgicale optimale.

The modern practice of awake craniotomy (AC) evolved with the development of sedative agents that facilitated existing local anesthetic techniques.1,2 This allowed the precise anatomic localization of neurologic function in patients who are undergoing supratentorial craniotomy, with most benefit seen predominantly for epilepsy surgery.3 Awake craniotomy with brain mapping has become the gold standard for patients undergoing surgery for tumours near or within eloquent areas of the brain. A wide variety of techniques have been described including the asleep-awake-asleep approach (SAS), monitored anesthesia care, and asleep-awake, awake-awake-awake, and conscious sedation approaches.4 Meng et al. recently succinctly summarized AC as a pre-awake, awake, and post-awake phase, with and without airway intervention.5 The goals include maintaining airway patency, optimizing cerebral perfusion, facilitating real-time brain mapping, minimizing postoperative pain, and allowing rapid recovery and assessment of neurologic function after surgery.6

Correlation between intraoperative neurologic testing (a, b), cortical area exposed at craniotomy (c), and functional magnetic resonance images (d, e)

Various anesthesia drugs have been used to achieve these goals, including propofol, remifentanil, fentanyl, and dexmedetomidine.7 The use of dexmedetomidine was first reported for AC surgery in 2001, predominantly as an adjunct to the SAS method, but with an additional benefit of decreased respiratory depression.8,9 While a propofol/remifentanil technique provides satisfactory conscious sedation, recognized drawbacks of this approach include hypoventilation and hypercapnia due to airway obstruction.10 Dexmedetomidine is a lipophilic imidazole derivative that acts as a selective pre- and post-synaptic alpha2 adrenoceptor agonist. It has anxiolytic, sedative, and anesthetic properties. Dexmedetomidine provides sedation that resembles natural sleep without cognitive impairment, making it an excellent anesthetic choice for AC surgery.11 An additional feature of dexmedetomidine making it attractive for AC surgery is its shorter arousal time compared with propofol.12 It has also been hypothesized that dexmedetomidine has a capacity to maintain the cerebral metabolic rate to cerebral blood flow (CBF) coupling. This results in a decrease in CBF, via an alpha2B receptor-mediated vasoconstriction, to match the reduced cerebral metabolic requirements during sedation and anesthesia.13,14 As research continues to elucidate the effect of dexmedetomidine on cancer cells, characterizing the impact of dexmedetomidine on tumour biology will be an important step in establishing the role of dexmedetomidine in neurooncology.15,16

In 2012, we instituted a standardized anesthetic technique of intravenous dexmedetomidine and scalp nerve blocks for patients undergoing AC surgery. This technique has been previously described by our group for select high-risk neurosurgical patients and is now the primary technique used at our institution.17,18 In this present study, we examined whether a dexmedetomidine-based sedation facilitates optimal conditions for AC defined as the avoidance of the need for airway manipulation or conversion to general anesthesia prior to complete brain mapping and brain tumour resection. Secondary outcomes included the establishment of optimal conditions for successful brain mapping and maximal tumour resection during AC.5


Eligibility and data collection

Following institutional Research Ethics Board approval in November 2016, waiving the need for patient consent, all adults (age ≥ 18 yr) who underwent AC at our institution during the study period from 1 March 2012 to 1 September 2016 were eligible for inclusion. Patients were excluded if their health records were incomplete or if they had a documented refusal of consent to participate in research. The intraoperative records of all patients who underwent AC surgery during the study period were screened for eligibility and, if applicable, data were extracted. Demographic and perioperative data collected included American Society of Anesthesiologists physical status (ASA-PS) classification, age, height, sex, weight, use of preoperative anti-epileptic drugs, tumour characteristics (pathology and location), and amplitude of direct cortical electrical stimulation (DCES), types and doses of anesthetic agents, intraoperative adverse events (airway manipulation or instrumentation, conversion to general anesthesia, nausea, and seizure activity), surgical outcomes (extent of resection and deviation of surgical plan based on preoperative functional magnetic resonance imaging), and select postoperative outcomes (new neurologic deficits, duration of hospital stay).

Anesthetic technique

Standard monitors were applied, intra-arterial blood pressure monitoring was instituted in all cases, and end-tidal carbon dioxide was monitored via a sampling channel integrated into a facemask or nasal cannula (depending on patient preference). A dexmedetomidine loading dose of 1 µg·kg−1 was administered over 15 min and an infusion started at 0.3-0.4 µg·kg−1·hr−1. Scalp nerve blocks were performed using an anatomical approach with 0.375% bupivacaine and epinephrine prior to pin insertion for both perioperative anesthesia and postoperative pain.19,20 Midazolam (0.01-0.05 mg·kg−1) and fentanyl (1 µg·kg−1) were administered before performance of the scalp blocks.

The patient was positioned awake and a Mayfield frame was used in all cases with supplemental lidocaine applied to the pin sites prior to insertion. The incision line was infiltrated with 2% lidocaine and additional infiltration of the muscle and topical anesthesia of the dura were performed by the surgeon as required throughout the case. The dexmedetomidine infusion rate was titrated to achieve a Ramsey sedation score between 2 and 4 until the dura was opened.21 Bolus doses of dexmedetomidine (0.05 µg·kg−1-0.1 µg·kg−1) were permitted throughout the case and infusion rates were increased as necessary to achieve required levels of sedation. Fentanyl for analgesia during bone flap and dural opening were provided at the discretion of the anesthesiologist; if required, a low-dose remifentanil infusion was permitted for supplemental analgesia. All infusions were discontinued at dural opening and restarted following neurophysiologic testing on a case-by-case basis. Hydromorphone, for postoperative analgesia, was administered following completion of the “awake” phase.

Neurologic assessment

Patient assessment involved pre- and postoperative neurophysiologic testing using a battery of tests for speech and cognition, including phenomic word fluency using the letters F, A, and S, semantic fluency tests (animal naming),22 the line bisection test,23 trail making tests A and B,24 the Weschler Memory Scale-Logical Stories (Anna Thompson story)25 judgement of line orientation,26 digit span, digit symbol, Rey-Osterreith Complex Figure,27 Barthel Index,28 Hospital Anxiety and Depression Scale,29 and Patient Assessment of Own Functioning.30

All patients underwent intraoperative speech and sensorimotor testing, which was dictated by the location of the tumour and of the cortical areas exposed by the craniotomy. Speech testing included number counting, naming, and word-generation tasks. Mapping was performed using bipolar Direct Cortical Electrical Stimulation [DCES with the OCS2 Ojemann Cortical Stimulator (Integra Life Sciences; Plainsborough, NJ, USA)]. Stimulation was performed with 500-msec pulses at 60 Hz with a starting amplitude of 2 mA and peak amplitude of 8mA31 (Figure).

Primary and secondary outcomes

The primary outcome was the incidence of failure of the AC anesthetic technique, defined by the need to convert to general anesthesia with a secured airway prior to (or during) brain mapping and brain tumour resection. Secondary outcomes were the incidence of: 1) optimal conditions for successful brain mapping and maximal tumour resection, 2) interventions to restore airway patency or rescue the airway, 3) significant (> 20% from baseline) hemodynamic instability, 4) nausea and vomiting, 5) new-onset neurologic deficits, and 6) seizure activity.

Statistical analysis

Data distribution was tested for normality using the Shapiro-Wilk test. Continuous data are presented as mean [standard deviation (SD)] when normally distributed or median (interquartile range [IQR]) when not normally distributed; categorical data were presented as proportions. The 95% confidence intervals are reported where appropriate. Fisher’s exact test was used to test differences between groups. P < 0.05 was considered statistically significant. All statistical analyses were performed using STATA 14 (STATACorp LP, TX, USA).


We identified 56 patients who underwent AC surgery during the study time period. One patient chart was excluded because of an incomplete health record. Fifty-five patients were included in the cohort, including ten patients described previously by Garavaglia et al.17 Demographic and intraoperative characteristics are summarized in Table 1. Most patients were male (55%), ASA-PS ≥ III (99%), and had preoperative seizure activity (64%) requiring anti-epileptic medication. The median [IQR] patient postoperative hospital stay was 2 [1-3] days.
Table 1

Demographic and intraoperative characteristics for all (n = 55) patients


n = 55

Age, yr

46 (16)

Male, n

30 (55%)

BMI (kg·m−2)

26 (6)

ASA classification, n



31 (56%)


23 (42%)

Preoperative seizures

35 (64%)

Intraoperative mannitol given, n

3 (5%)

Systolic blood pressure (mmHg)



151 (18)


108 (14)

Heart rate (beats·min−1)



76 (12)


54 (8)

Maximum PaCO2 (mmHg)

41 (8)

Duration in minutes

230 [190 – 309]

Postoperative length of hospital stay

2 [1-3]

Data are represented by as mean (standard deviation), median [interquartile range], or percentage (%) as indicated

ASA = American Society of Anesthesiologists; BMI = body mass index; PaCO2 = partial pressure of carbon dioxide

Primary outcomes

All patients included in the study underwent successful AC with DCES for motor or speech function. There was no failure of the approach requiring conversion to general anesthesia with a secured airway. No intraoperative interventions were required to restore airway patency.

Secondary outcomes

The preoperative functional MRI-based surgical plan was often modified using intraoperative information acquired from DCES. Modifications to this plan fell into three categories: 1) identification of the corridor for tumour resection [17/55 (31%)], 2) definition of the limit of resection [31/55 (56%)], and 3) identification of the focus of positive stimulation distant from the corridor or site of tumour resection [6/55 (11%)]. In patients in the third category, our practice was to keep patients awake throughout the phase of tumour resection, often with serial episodes of cortical or subcortical stimulation during physiologic testing. Overall, 17/55 (31%) of patients remained awake throughout the process of tumour resection. The remainder underwent some degree or duration of deep sedation following the brain mapping.

Intraoperative medications administered are described in Table 2. Mean (SD) time from commencement of dexmedetomidine infusion to first cessation for testing was 100 (33) min. The mean (SD) cumulative dose of dexmedetomidine administered prior to initiating neurophysiologic testing was 1.80 (0.76) µg·kg−1. Fentanyl and midazolam were predominantly administered prior to pinning with supplemental fentanyl administered at dural opening as needed. Hydromorphone loading for postoperative analgesia took place following completion of testing in the majority of cases. In 7/55 (13%) of patients, hydromorphone was administered prior to testing in a dose range 0.002-0.13 mg·kg−1. Mean (SD) intraoperative hydromorphone dose administered in all patients was 1.2 (0.6) mg.
Table 2

Mean (SD) doses of anesthetic and analgesic medications administered


Prior to Neurophysiologic Testing

Total Intraoperative Dose

Total dexmedetomidine dose (mg·kg−1)

1.80 (0.76)

2.4 (1.0)

Bolus dexmedetomidine dose (mg·kg−1)

0.80 (0.6)

0.13 (0.09)

Midazolam (mg)/per patient

2 (1)

2.1 (1.3)

Fentanyl (µg)/per patient

101 (65)

106 (71)

Hydromorphone (mg)/per patient

0.08 (0.25)

1.2 (0.6)

SD = standard deviation

No significant changes in blood pressure were observed related to dexmedetomidine use. One patient experienced an episode of bradycardia associated with hypotension at dural opening, which responded to bolus glycopyrolate (0.2 mg). At the time of the episode, the infusion dose of dexmedetomidine was 1 µg·kg−1·hr−1. There were no nausea and vomiting during the procedure. Only one patient required low-dose supplemental remifentanil infusion at a rate of 0.005-0.02 µg·kg−1·min−1 for analgesia during the initial period up to dural opening. Emergence agitation or delirium was not evident in any patient and no patient required general anesthesia after the initial pre-awake phase.

Tumour characteristics and surgical outcomes are summarized in Table 3. There were no episodes of generalized seizure. Focal seizures induced by DCS occurred in nine (16%) patients, of which eight (15%) occurred in patients with pre-existing preoperative seizure activity on anti-epileptic medication. All occurred at the time of cortical stimulation. Seizures resolved with direct administration of cold saline alone in seven (13%) patients; two patients required midazolam (0.5 mg) and phenytoin after mapping to control focal seizure activity. None of the events required premature termination of cortical mapping and no seizure resulted in airway intervention or conversion to general anesthesia. There was no association between preoperative antiepileptic use and intraoperative seizures (P > 0.99) or between intraoperative phenytoin use and intraoperative seizures (P = 0.69). Characteristics of seizure activity are summarized in Table 4. Gross total resection of metastatic lesions, the area of enhancement in high-grade glioma cases, or the area of FLAIR signal abnormality in low-grade gliomas cases was achieved in 32 (56%) patients. Three patients (5%) developed new postoperative neurologic deficits following surgery, one of which was associated with a postoperative hemorrhage within the tumour cavity.
Table 3

Tumour characteristics and surgical outcomes for all (n = 55) patients


n (%)

Tumour pathology

 High-grade tumour

25 (46)

 Low-grade tumour

29 (53)


1 (2)

Tumour site


34 (62)


13 (24)


8 (15)

Positive stimulation achieved

45 (82)

Change in surgical plan due to DCES

13 (24)

1) Limit of resection

31 (56)

2) Corridor for resection

17 (31)

3) Resection distant from DCES site

6 (11)

Gross total resection achieved

32 (56)

New postoperative neurologic deficit

3 (5)

DCES = direct cortical electrical stimulation

Table 4

Incidence of intraoperative seizure activity, classified by anticonvulsant use and tumour pathology


Stimulation-induced Seizures (n = 9)

No Seizures (n = 46)

P value

Preoperative anticonvulsant use, n

6 (67%)

29 (63%)

> 0.99

Perioperative phenytoin, n

1 (11%)



Tumour pathology, n



 High grade

3 (33%)

23 (50%)


 Low grade

4 (45%)

14 (30%)



1 (11%)

7 (15%)



1 (11%)

2 (5%)



We describe our experience of using a predominantly dexmedetomidine-based anesthetic technique in conjunction with scalp blocks to facilitate AC surgery. This technique shows that dexmedetomidine can be used as the primary anxiolytic and sedative drug for AC surgery up to four hours in duration with no adverse respiratory events and providing optimal neurosurgical conditions. In our cohort, using dexmedetomidine anesthesia, no patient required unplanned airway intervention or conversion to a general anesthesia.

Our reported outcomes are in keeping with the relatively low conversion rates to GA utilizing other anesthetic protocols. Previously published anesthesia failure rates during AC surgery vary, but typically 2-6% of patients require some form of airway manipulation during AC.32 The reasons for airway interventions generally include poor patient selection, an inadequate anesthetic regimen, and intraoperative stimulation-induced seizures. The choice of anesthetic technique influences perioperative adverse events. Goettel et al. found no respiratory events when dexmedetomidine/propofol was used for rescue, but 20% with propofol/remifentanil.33 Dilmen et al. more recently reported moderate-to-severe intraoperative desaturations in almost 20% of cases using a dexmedetomidine-based technique, but with unquantified amounts of remifentanil or propofol suplementation.34 Our study adds to the evidence base, suggesting that use of dexmedetomidine without propofol can be safely performed with no adverse respiratory events, no conversion to general anesthesia, and successful intraoperative mapping throughout. Lobo et al. have suggested that for surgeries with an expected duration exceeding four hours, the SAS technique is more appropriate as patients can cooperate better if their awake phase is preceded by an asleep phase. Concern has also been expressed regarding potential accumulation of dexmedetomidine and delayed return of function in prolonged procedures.35 The median duration of surgery in our study was less than four hours, and there were no deleterious effects on intraoperative mapping or delayed return of function observed.

Awake surgery offers the best approach to optimal tumour removal while minimizing the risk of permanent postoperative neurologic deficits, with both improved quality of life and prolonged survival.36 In a number of our cases, the operative plan was modified based on unexpected findings during stimulation of eloquent brain regions within the planned area of tumour resection. In these cases, tumour resection was minimized to optimize intact neurologic function. This finding strongly suggests a benefit to continued patient assessment during tumour resection. The low rate (5%) reported here of new postoperative neurologic deficits following surgery, despite aggressive tumour resection, also compares favorably with other studies. A recent systematic review found a 7% incidence of new focal deficit after AC but 23% after general anesthesia.37 Similarly, Honorato-Cia et al. found significantly lower perioperative neurologic deficits using a predominantly dexmedetomidine-based approach (in a dose range of 0.2-1.4 µg·kg−1·min−1) compared with other techniques.38 Dilmen et al. also reported reduced postoperative neurologic deficits using conscious sedation compared with SAS.34

While other studies have previously shown dexmedetomidine to be effective for AC surgery, the use of supplementary propofol—by either infusion or bolused—was most often used.39

The use of midazolam in AC is controversial, as it can be associated with emergence agitation and delirium when transitioning to the awake phase.6 This was not noted in our cohort where 52 (95%) patients received midazolam perioperatively. A mean (SD) dose of 2 mg (1) was administered prior to neurophysiologic testing. In animal studies, midazolam has been shown to interact synergistically with dexmedetomidine resulting in a dose-sparing effect.40 The ability to use lower doses of dexmedetomidine to achieve sedation may have some benefits in reducing the side effects of dexmedetomidine and did not interfere with neurocognitive testing in this cohort. A recent study by Suero Molina et al. comparing dexmedetomidine and remifentanil to an SAS technique for AC found that dexmedetomidine did result in better quality and reliable neurologic testing upon cessation.41

One of the main criticisms of using dexmedetomidine is the potential for blunting of the carbon dioxide (CO2) response curve,42 and some anesthesiologists advocate for advanced airways for the pre-awake phase to minimize this risk. This is an important consideration for those patients with a “tight brain” and increased surgical difficulty. Despite this, hypercapnia, due to either obstruction or hypoventilation, was not found in this cohort. Indeed, the mean (SD) maximal partial pressure of carbon dioxide was very near physiologic levels of 40 mmHg,8 suggesting that the central physiologic responsiveness to CO2 was maintained. In addition, favorable brain tension was reported in the vast majority of cases in this study. Previous reports of dose-related cardiovascular effects have described episodes of bradycardia of up to 27% during AC surgery,43 but within this cohort we found no clinically significant hypotension and only one episode of bradycardia with a surgical etiology requiring treatment.

Surgical failure during AC is defined as incomplete intraoperative awake monitoring of brain function during tumour resection, typically reported at approximately 2%.44 Nonetheless, even with a continuously awake (i.e., awake-awake-awake) approach, there is still an inherent failure rate (approximately 2%) due to seizure activity.45 Seizures have historically been the major cause of aborted AC surgery with reported incidences in the range of 3-22%. Nevertheless, phenytoin use is also associated with communication and AC failure, with no evidence of reducing perioperative seizure activity.46 The seizure rate in our cohort was comparable to previous studies, and all seizures were triggered by cortical stimulation with most terminated with the application of cold saline.

Our study has some limitations. The retrospective nature of this study introduces several risks of bias and missing data. The surgical team provided information on alterations to the surgical plan following retrospective assessment of patient charts, which may have introduced recall bias. In addition, total doses of local anesthetics used by the surgical team were inconsistently recorded and could not be reported. In addition, formal pain and discomfort scores were not recorded for all patients. As AC surgery is relatively uncommon, there were insufficient data available prior to 1 March 2012 to make a comparison with non-dexmedetomidine anesthesia in our convenience sample.


Awake craniotomy for tumour resection using a dexmedetomidine-based anesthetic and scalp blocks resulted in no airway complications or conversion to general anesthesia. The anxiolytic and analgesic properties of dexmedetomidine enabled patients to remain awake and be surveilled during tumour resection. Further evaluations of clinical outcomes associated with this approach could include the duration of disease-free survival, time to tumour recurrence, and overall quality of life.


Conflict of interest

The authors have no conflicts of interest to disclose.

Editorial responsibility

This submission was handled by Dr. Hilary P. Grocott, Editor-in-Chief, Canadian Journal of Anesthesia.

Author contributions

Niamh McAuliffe was involved in the study design, ethics approval, data analysis, and manuscript preparation. Stuart Nicholson was involved in the data acquisition and data analysis. Andrea Rigamonti and Marco Garavaglia were involved in the manuscript preparation. Gregory M.T. Hare was involved in the study design and manuscript preparation. Michael Cusimano was involved in the data acquisition and manuscript preparation. Iryna Pshonyak was involved in the data collection. Sunit Das was involved in the study design, data collection, and manuscript preparation.


This project was not supported by any funding. GH is supported by a Merit Award from the Department of Anesthesia, University of Toronto. DS received funding from the Canadian Cancer Society. Research Ethics Board Approval Number: 16-313.


  1. 1.
    Bulsara KR, Johnson J, Villavicencio AT. Improvements in brain tumor surgery: a modern history of awake craniotomy. Neurosurg Focus 2005; 18: e5.PubMedGoogle Scholar
  2. 2.
    Archer DP, McKenna JM, Morin L, Ravussin P. Conscious-sedation analgesia during craniotomy for intractable epilepsy: a review of 354 consecutive cases. Can J Anaesth 1988; 35: 338-44.CrossRefPubMedGoogle Scholar
  3. 3.
    Penfield W. Combined regional and general anesthesia for craniotomy and cortical exploration. I. Neurosurgical considerations. Curr Res. Anesth Analg 1954; 33: 145-55.CrossRefGoogle Scholar
  4. 4.
    Olsen KS. The asleep-awake technique using propofol-remifentanil anaesthesia for awake craniotomy for cerebral tumours. Eur J Anaesthesiol 2008; 25: 662-9.CrossRefPubMedGoogle Scholar
  5. 5.
    Meng L, McDonagh DL, Berger MS, Gelb AW. Anesthesia for awake craniotomy: a how-to guide for the occasional practitioner. Can J Anesth 2017; 64: 517-29.CrossRefPubMedGoogle Scholar
  6. 6.
    Gruenbaum SE, Meng L, Bilotta F. Recent trends in the anesthetic management of craniotomy for supratentorial tumor resection. Curr Opin Anaesthesiol 2016; 29: 552-7.CrossRefPubMedGoogle Scholar
  7. 7.
    Prontera A, Baroni S, Marudi A, et al. Awake craniotomy anesthetic management using dexmedetomidine, propofol, and remifentanil. Drug Des Devel Ther 2017; 11: 593-8.CrossRefPubMedPubMedCentralGoogle Scholar
  8. 8.
    Bekker AY, Kaufman B, Samir H, Doyle W. The use of dexmedetomidine infusion for awake craniotomy. Anesth Analg 2001; 92: 1251-3.CrossRefPubMedGoogle Scholar
  9. 9.
    Ard JL Jr, Bekker AY, Doyle WK. Dexmedetomidine in awake craniotomy: a technical note. Surg Neurol 2005; 63: 114-6.CrossRefPubMedGoogle Scholar
  10. 10.
    Herrick IA, Craen RA, Gelb AW, et al. Propofol sedation during awake craniotomy for seizures: patient controlled administration versus neurolept analgesia. Anesth Analg 1997; 84: 1285-91.CrossRefPubMedGoogle Scholar
  11. 11.
    Rozet I. Anaesthesia for functional neurosurgery: the role of dexmedetomidine. Curr Opin Anaesthesiol 2008; 21: 537-43.CrossRefPubMedGoogle Scholar
  12. 12.
    Shen SL, Zheng JY, Zhang J, et al. Comparison of dexmedetomidine and propofol for conscious sedation in awake craniotomy: a prospective, double-blind, randomized, and controlled clinical trial. Ann Pharmacother 2013; 47: 1391-9.CrossRefPubMedGoogle Scholar
  13. 13.
    Prielipp RC, Wall MH, Tobin JR, et al. Dexmedetomidine-induced sedation in volunteers decreases regional and global cerebral blood flow. Anesth Analg 2002; 95: 1052-9.PubMedGoogle Scholar
  14. 14.
    Drummond JC, Dao AV, Roth DM, et al. Effect of dexmedetomidine on cerebral blood flow velocity, cerebral metabolic rate, and carbon dioxide response in normal humans. Anesthesiology 2008; 108: 225-32.CrossRefPubMedGoogle Scholar
  15. 15.
    Luo X, Zheng X, Huang H. Protective effects of dexmedetomidine on brain function of glioma patients undergoing craniotomy resection and its underlying mechanism. Clip Neurol Neurosurg 2016; 146: 105-8.CrossRefGoogle Scholar
  16. 16.
    Zhang F, Ding T, Yu L, Zhong Y, Dai H, Yan M. Dexmedetomidine protects against oxygen-glucose deprivation-induced injury through the I2 imidazoline receptor-PI3K/AKT pathway in rat C6 glioma cells. J Pharm Pharmacol 2012; 64: 120-7.CrossRefPubMedGoogle Scholar
  17. 17.
    Garavaglia MM, Das S, Cusimano MD, et al. Anesthetic approach to high-risk patients and prolonged awake craniotomy using dexmedetomidine and scalp block. J Neurosurg Anesthesiol 2014; 26: 226-33.CrossRefPubMedGoogle Scholar
  18. 18.
  19. 19.
    Guilfoyle MR, Helmy A, Duane D, Hutchinson PJ. Regional scalp block for postcraniotomy analgesia: a systematic review and meta-analysis. Anesth Analg 2013; 116: 1093-102.CrossRefPubMedGoogle Scholar
  20. 20.
    Rigamonti A, Garavaglia M, Hanlon J, et al. Effect of bilateral scalp nerve blocks on post-operative pain in patients undergoing supratentorial craniotomy and general anaesthesia. Anesthesiology 2012; 38: A462.Google Scholar
  21. 21.
    Sessler CN, Gosnell MS, Grap MJ, et al. The Richmond Agitation-Sedation Scale: validity and reliability in adult intensive care unit patients. Am J Respir Crit Care Med 2002; 166: 1338-44.CrossRefPubMedGoogle Scholar
  22. 22.
    Tombaugh TN, Kozak J, Rees L. Normative data stratified by age and education for two measures of verbal fluency: FAS and naming. Arch Clin Neurophyschol 1999; 14: 167-77.Google Scholar
  23. 23.
    Ferber S, Karnath HO. How to assess spatial neglect-line bisection or cancellation tasks? J Clin Exp Neuropsychol 2001; 23: 599-607.CrossRefPubMedGoogle Scholar
  24. 24.
    Bowie CR, Harvey PD. Administration and interpretation of the Trail Making Test. Nat Protoc 2006; 1: 2277-81.CrossRefPubMedGoogle Scholar
  25. 25.
    Elwood RW. The Wechsler Memory Scale-revised: psychometric characteristics and clinical application. Neuropsychol Rev 1991; 2: 179-201.CrossRefPubMedGoogle Scholar
  26. 26.
    Spencer RJ, Wendell CR, Giggey PP, Seliger SL, Katzel L, Waldstein SR. Judgment of line orientation: an examination of eight short forms. J Clin Neuropsychol 2013; 35: 160-6.CrossRefGoogle Scholar
  27. 27.
    Shin MS, Park SY, Park SR, Seol SH, Kwon JS. Clinical and empirical applications of the Rey-Osterrieth Complex Figure Test. Nat Protoc 2006; 1: 892-9.CrossRefPubMedGoogle Scholar
  28. 28.
    Mahoney FI, Barthel DW. Functional evaluation: the Barthel Index. Md State Med J 1965; 14: 61-5.PubMedGoogle Scholar
  29. 29.
    Bjelland I, Dahl AA, Haug TT, Neckelmann D. The validity of the Hospital Anxiety and Depression Scale. An updated literature review. J Psychosom Res 2002; 52: 69-77.CrossRefPubMedGoogle Scholar
  30. 30.
    Chelune GJ, Heaton RK, Lehman RA. Neuropsychological and personality correlates of patients’ complaints of disability. Adv Clin Neuropsychol 1986; 3: 95-126.CrossRefGoogle Scholar
  31. 31.
    De Witt Hamer PC, Robles SG, Zwinderman AH, Duffau H, Berger MS. Impact of intraoperative stimulation brain mapping on glioma surgery outcome: a meta-analysis. J Clin Oncol 2012; 30: 2559-65.CrossRefPubMedGoogle Scholar
  32. 32.
    Hervey-Jumper SL, Li J, Lau D, et al. Awake craniotomy to maximize glioma resection: methods and technical nuances over a 27-year period. J Neurosurg 2015; 123: 325-39.CrossRefPubMedGoogle Scholar
  33. 33.
    Goettel N, Bharadwaj S, Venkatraghavan L, Mehta J, Bernstein M, Manninen PH. Dexmedetomidine vs propofol-remifentanil conscious sedation for awake craniotomy: a prospective randomized controlled trial. Br J Anaesth 2016; 116: 811-21.CrossRefPubMedGoogle Scholar
  34. 34.
    Dilmen OK, Akcil EF, Oguz A, Vehid H, Tunali Y. Comparison of conscious sedation and asleep-awake-asleep techniques for awake craniotomy. J Clin Neurosci 2017; 35: 30-4.CrossRefPubMedGoogle Scholar
  35. 35.
    Lobo FA, Wagemakers M, Absalom AR. Anaesthesia for awake craniotomy. Br J Anaesth 2016; 116: 740-4.CrossRefPubMedGoogle Scholar
  36. 36.
    Grossman R, Nossek E, Sitt R, et al. Outcome of elderly patients undergoing awake-craniotomy for tumor resection. Ann Surg Oncol 2013; 20: 1722-8.CrossRefPubMedGoogle Scholar
  37. 37.
    Brown T, Shah AH, Bregy A, et al. Awake craniotomy for brain tumor resection: the rule rather than the exception? J Neurosurg Anesthesiol 2013; 25: 240-7.CrossRefPubMedGoogle Scholar
  38. 38.
    Honorato-Cia C, Martinez-Simón A, Guridi J, Alegre M, Nuñez-Cordoba JM. Sedation during surgery for movement disorders and perioperative neurologic complications: an observational study comparing local anaesthesia, remifentanil, and dexmedetomidine. World Neurosurg 2017; 101: 114-21.CrossRefPubMedGoogle Scholar
  39. 39.
    Venkatraghavan L, Bharadwaj S, Au K, Bernstein M, Manninen P. Same-day discharge after craniotomy for supratentorial tumour surgery: a retrospective observational single-centre study. Can J Anesth 2016; 63: 1245-57.CrossRefPubMedGoogle Scholar
  40. 40.
    Boehm CA, Carney EL, Tallarida RJ, Wilson RP. Midaxolam enhances the analgesic properties of dexmedetomidine in the rat. Vet Anaesth Analg 2010; 37: 550-6.CrossRefPubMedPubMedCentralGoogle Scholar
  41. 41.
    Suero Molina E, Schipmann S, Mueller I, et al. Conscious sedation with dexmedetomidine compared with asleep-awake-asleep craniotomies in glioma surgery: an analysis of 180 patients. J Neurosurg 2018; 12: 1-8.CrossRefGoogle Scholar
  42. 42.
    Nishida T, Nishimura M, Kagawa K, Hayashi Y, Mashimo T. The effects of dexmedetomidine on the ventilatory response to hypercapnia in rabbits. Intensive Care Med 2002; 28: 969-75.CrossRefPubMedGoogle Scholar
  43. 43.
    Bhana N, Goa KL, McClellan KJ. Dexmedetomidine. Drugs 2000; 59: 263-8.CrossRefPubMedGoogle Scholar
  44. 44.
    Stevanovic A, Rossaint R, Veldeman M, Bilotta F, Coburn M. Anaesthesia management for awake craniotomy: systematic review and meta-analysis. PLoS One 2016; 11: e0156448.CrossRefPubMedPubMedCentralGoogle Scholar
  45. 45.
    Seemann M, Zech N, Graf B, Hansen E. Anesthesiological management of awake craniotomy: asleep-awake-asleep technique or without sedation (German). Anaesthetist 2015; 64: 128-36.CrossRefGoogle Scholar
  46. 46.
    Nossek E, Matot I, Shahar T, et al. Failed awake craniotomy: a retrospective analysis in 424 patients undergoing craniotomy for brain tumor. J Neurosurg 2013; 118: 243-9.CrossRefPubMedGoogle Scholar

Copyright information

© Canadian Anesthesiologists' Society 2018

Authors and Affiliations

  1. 1.Department of Anesthesiology, St. Michael’s HospitalUniversity of TorontoTorontoCanada
  2. 2.Division of Neurosurgery, St. Michael’s HospitalUniversity of TorontoTorontoCanada
  3. 3.Li Ka Shing Knowledge Institute and Keenan Research Centre for Biomedical ResearchTorontoCanada
  4. 4.Department of PhysiologyUniversity of TorontoTorontoCanada

Personalised recommendations