International Journal of Surgery 36 (2016) 454e459

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International Journal of Surgery

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Anesthesia considerations in epilepsy surgery

Anita Shetty a, *, Swarada Pardeshi b, Viraj M. Shah b, Aarti Kulkarni b
a
Neuroanesthesia Fellowship Programme, Department of Anesthesia, Seth GS Medical College & KEM Hospital, Mumbai, India
b
Department of Anesthesia, Seth GS Medical College & KEM Hospital, Mumbai, India

h i g h l i g h t s

Preoperative evaluation.

Proconvulsant and anticonvulsant effects of anesthetic agents.

Anesthetic techniques for temporal lobe epilepsy.

Vagal nerve stimulation.

Cerebral hemispherectomy and corpus callosotomy.

a r t i c l e i n f o a b s t r a c t

Article history: Epilepsy surgeries can be done under general anesthesia or with local anesthesia and sedation. Epilepsy
Received 4 May 2015 surgery done under general anesthesia have similar goals as any other neurosurgical procedure, except in
Received in revised form patients with temporal lobe epilepsy requiring cortical mapping or electrocorticography (ECoG) where
28 June 2015
depth of anesthesia has to be reduced. Since seizure focus localization can be done preoperatively with
Accepted 14 July 2015
Available online 15 July 2015
modern diagnostic tools, general anesthesia is popular even for these patients. It is comfortable for both
the surgeon and the patient. For intraoperative ECoG or cortical mapping awake craniotomy is the
preferred technique.
Keywords:
Epilepsy surgery
© 2015 IJS Publishing Group Ltd. Published by Elsevier Ltd. All rights reserved.
Anesthesia management
Awake craniotomy
Electrocorticography

1. Introduction 2. Preoperative evaluation [1e3]

Surgery for epilepsy requires a multidisciplinary approach from
the neurosurgeon, the neurophysician, the neurophysiologist and
the neuroanesthetist. The various types of surgeries for epilepsy
include electrode placement, resection surgery, disconnections and
placement of seizure modulation device.
Epilepsy surgery poses significant challenges to the neuro-
anesthetist. The challenges are to provide optimal operating
conditions, hemodynamic stability, monitored anesthesia care
for awake craniotomy and rapid emergence for neurological
assessment as well as avoidance of agents which interfere with
intraoperative ECoG (electrocorticography) and cortical
mapping.
* Corresponding author.
E-mail address: anitanshetty@yahoo.co.uk (A. Shetty).
Many disorders are associated with epilepsy which must be
evaluated and optimized preoperatively. Patients with epilepsy are
on chronic anticonvulsant therapy which can adversely affect
various systems and have drug interactions. Table 1 summarizes
the preoperative conditions and its anesthetic implications.
3. Preoperative preparation
Patients must be prepared psychologically for surgery especially
if awake craniotomy is planned. The effects of intraoperative testing
like nausea due to traction on the temporal lobe and likelihood of
intraoperative seizures must be explained. Psychological support
must be given to patients who have associated affective and per-
sonality disorders [1]. Patients must be informed about the possi-
bility of intraoperative awareness during general anesthesia, as
anesthetic depth may be lightened during ECoG monitoring.

http://dx.doi.org/10.1016/j.ijsu.2015.07.006
1743-9191/© 2015 IJS Publishing Group Ltd. Published by Elsevier Ltd. All rights reserved.
 A. Shetty et al. / International Journal of Surgery 36 (2016) 454e459 455

Table 1
Preoperative evaluation.

Condition Anesthetic implications

Von Recklinghausen's disease (neurofibromatosis) Intracranial tumor

Tuberous sclerosis
Chronic anticonvulsant therapy
Craniotomy for placement of intracranial electrodes
Compromised pulmonary system due to chronic aspiration, fibrosing alveolitis and pulmonary hypertension.
Atlanto-axial instability
Increased sensitivity to neuromuscular blocking drugs.
Associated cardiac arrhythmias, cardiac tumors as well as renal and respiratory dysfunction.
Increased metabolism of opioids and non- depolarising muscle relaxants
Phenytoin causes gingival hyperplasia which may make airway difficult.
Carbamazepine can suppress hematopoietic system and cause cardiac toxicity.
Sodium valproate causes thrombocytopenia and platelet dysfunction.
Sedative side effects may increase the depressive effects of anesthetic agents.
Pneumocephalus may persist upto three weeks. Nitrous oxide avoided.

4. Premedication
Table 2
Benzodiazepines must be avoided if intraoperative ECoG is Proconvulsant and anticonvulsant effects of anesthetic agents in epileptic patients
[5,6,12,15].
planned. Antiepileptics can be administered on the morning of
surgery after consultation with the neurophysician and Agent Proconvulsant Anticonvulsant
neurosurgeon. Intravenous agents
Thiopental e þ
Methohexital þ þ
5. Proconvulsant and anticonvulsant effects of anesthetic
Etomidate þ þ
agents Ketamine þ þ
Propofol e þ
Reports on the effects of anesthetic agents as proconvulsant and Benzodiazepines e þ
Inhalational agents
anticonvulsant are conflicting and inconclusive.
Nitrous Oxide e e
At different doses most of the anesthetics have proconvulsant Halothane þ þ
and anticonvulsant effects. Ratio of excitatory and inhibitory neu- Enflurane e þ
rons change with the depth of sedation. As the depth increases Isoflurane þ þ
alpha waves are replaced with high frequency beta activity which Sevoflurane e ?
Desflurane e þ
progresses to high amplitude low frequency theta and delta waves.
During intraoperative ECoG it is important to maintain low depth of (þ) e present, () e absent, (?) e Information not available.
Proconvulsant e Provoke seizures. Anticonvulsant-suppress status epilepticus.
anesthesia [4].
Intravenous induction agents such as barbiturates (thiopental
and methohexital) and propofol have been used to treat refractory
status epilepticus. They also produce myoclonus, opisthotonus and [10]. It does not affect spikes. These properties make it favorable for
rarely generalized seizures during induction of anesthesia. All these use in awake craniotomy for epileptic patient [11].
agents are anticonvulsants at higher doses [5]. Inhalational agents such as halothane, isoflurane and desflurane
Thiopentone and propofol are not associated with epileptiform have no proconvulsant properties when used alone. Isoflurane and
activities on EEG whereas methohexital and etomidate are associ- desflurane have been used to treat refractory status epilepticus
ated with EEG evidence of epileptiform activity in patients with [12]. Nitrous oxide does not have anticonvulsant or proconvulsant
temporal lobe epilepsy [1]. Thiopentone and benzodiazepines are properties. Nitrous oxide when added to propofol or isoflurane can
potent anticonvulsants [1,6]. Reports about the effects of propofol suppress the ECoG [13]. Concentration of isoflurane between 0.25
on ECoG are conflicting. In epileptic patients low doses of propofol and 1.25% along with 50e70% nitrous oxide does not affect the
activated electrocorticogram and high dose produced burst sup- spike activity [14]. Enflurane had EEG documented spikes as well as
pression [7]. There has been a report of activation of epileptogenic myoclonus when high concentration was used along with hypo-
foci after administering a bolus of propofol (2 mg/kg, IV), in patient capnia [1,15]. In patients with epilepsy EEG evidence of seizure
having history of intractable temporal lobe epilepsy which lasted activity has been noticed during sevoflurane anesthesia [16]. In
for upto 7 min [6]. Numerous studies have shown that propofol is epilepsy surgeries, sevoflurane with other anesthetic agents may
safe for use in epilepsy surgeries. During emergence from pro- suppress spikes [17]. Sevoflurane causes widespread nonspecific
longed propofol infusion marked beta activity may obscure the EEG spikes which do not help in localization of epileptiform focus [18]
[8]. It does not interfere with ECoG if stopped minimum 15 min (Table 2).
prior to recording [9]. Etomidate, methohexital and ketamine can None of the neuromuscular blocking agents or anticholines-
activate EEG activity when administered to patients with epilepsy terase agents affect EEG or clinical seizure activity [6].
surgery. These may help to localize the ictal foci. Intravenous ke- The different types of epilepsy surgeries done are
tamine activates either cortical EEG or clinical seizure activity in
epileptics when >2 mg/kg is administered [6] (Table 2).
Electrode placement e strips and grids.
Low bolus dose or infusion of opioids have no effect on spikes.
Resection surgery e amygdalohippocampectomy, temporal lo-
Large bolus doses of synthetic opioids like fentanyl, sufentanil, bectomy and anatomical hemispherectomy.
alfentanil, remifentanil can activate inter-ictal spikes. Morphine has
Disconnections e corpus callosotomy, multiple subpial tran-
no proconvulsant effect. Meperidine can induce seizures due to its section and functional hemispherectomy.
metabolite normeperidine [6].
Placement of seizure modulation device evagal nerve
Dexmedetomidine is an alpha- 2 agonist, which produces anx- stimulation.
iolysis, analgesia and sedation without much respiratory depression
456 A. Shetty et al. / International Journal of Surgery 36 (2016) 454e459
6. Temporal lobe epilepsy
6.1. Anesthetic techniques
1. General anesthesia
2. Awake craniotomy
7. Surgery under general anesthesia
Identification of epileptogenic zone from which seizures
originate and its excision without complications is the primary
goal of epilepsy surgery. Anesthetic agents are known to alter
ECoG activity and thus the role of anesthesiologist becomes
important so that optimal waveforms are obtained for neurolo-
gist and neurosurgeon to perform resection. The challenge
further lies in avoiding awareness during intraoperative ECoG
and motor testing while keeping the influence of anesthetics to a
minimum.
The use of general anesthesia for resection of epileptogenic foci
without brain mapping (anterior temporal lobectomy) or ECoG
monitoring has similar anesthetic goals as most open craniotomy
procedures. During cortical mapping or ECoG guided resection,
depth of anesthesia should be reduced.
Intraoperative monitoring depends on the type of surgery and
extent of resection. Routine monitoring is usually sufficient in a
majority of cases.
Induction can be done with intravenous agents such as propofol
and fentanyl. Total intravenous anesthesia using propofol or inha-
lational agents like isoflurane or desflurane can be safely used for
maintenance of anesthesia as they do not show evidence of acti-
vation of spikes [4].
Stopping or weaning of intravenous and inhalation agents is
required prior to ECoG as they can suppress the spikes. Opioids
such as fentanyl and remifentanil also have no effect on background
ECoG, thus a low-dose bolus or continuous infusion can be
continued. Continuous infusion of Dexmedetomidine, can be used
intraoperatively as it has no effect on spikes. The use of nitrous
oxide during ECoG monitoring is controversial. Artru et al. [19]
reported that nitrous oxide suppresses focal epileptiform activity
during intraoperative ECoG. Hosain et al. [20] in a study of eighteen
epilepsy surgery patients, concluded that in routine concentration
nitrous oxide does not affect the interictal spikes and can be safely
used in epilepsy surgery.
At the time of ECoG recording, muscle relaxation must be pro-
vided to prevent patient movement. If cortical motor area stimu-
lation is required dosage of neuromuscular blocking drugs should
be minimal.
Intraoperative seizures can be treated by administering cold
Ringer lactate wash to brain [21], IV propofol bolus 10e30 mg or IV
midazolam 1e2 mg bolus [19]. Administration of drugs might
interfere with ECoG recording.
In case of failure to elicit intraoperative seizure spike on ECOG,
etomidate (0.2 mg/kg), alfentanil (0.02 mg/kg) or methohexital
(25e50 mg) can be administered to promote epileptiform dis-
charges [1].
8. Awake craniotomy
Awake craniotomy is preferred when the epileptic focus lies in
or near eloquent areas of brain or for better ECoG localization of
seizure focus without the influence of general anesthetic drugs.
Advantages of this technique include continuous neurologic
monitoring, better localization of seizure foci, shorter hospital stay
and lower incidence of postoperative anesthetic complications like
nausea and vomiting [22].
Anesthetic challenges of awake craniotomy are rapid and smooth
transition of anesthetic depth, maintenance of stable hemodynamics
and management of intraoperative complications [23].
9. Patient selection
Co-operative and motivated patients are ideal candidates. Pa-
tients with anxiety, psychiatric disorder and emotional instability
may not be suitable for awake craniotomy. Patients with antici-
pated difficult airway, obesity, gastro-esophageal reflux and
chronic cough are relative contraindications whereas obstructive
sleep apnea may be an absolute contraindication [22,24].
10. Monitoring
Standard monitoring is usually sufficient. The need for invasive
monitoring is decided on the basis of patient's comorbidities. Bis-
pectral index (BIS) can be used to monitor the level of sedation
during awake craniotomy. It can reduce the incidence of respiratory
depression [25]. BIS values correlated better with the level of
consciousness than effect-site concentration of propofol during
target-controlled infusion of propofol and remifentanil used for
awake craniotomy [26]. In patients on antiepileptic medications
there may be delay in increase in BIS value with increase in level of
consciousness, hence in these patients BIS values must be inter-
preted cautiously [27].
11. Positioning
Patient should be positioned comfortably. Lateral position is
most preferred as it provides easy access to airway and less chances
of airway obstruction. Drapes should be arranged in such a manner
that the patient does not feel claustrophobic. A view of the patient's
face and extremities is important for patient safety and adequate
sensory, motor, speech and memory testing. Patient should be
positioned on a soft mattress and pressure points should be padded
adequately.
12. Anesthetic techniques for awake craniotomy
12.1. Monitored anesthesia care
Scalp block is administered under light sedation. Target
controlled infusions of propofol, opioids or dexmedetomidine can
be used. Once the dura is opened, low-dose infusion of remifentanil
or dexmedetomidine can be continued to perform the testing.
Propofol must be stopped at least 15 min prior to testing or cortical
mapping [9]. Patient breathes spontaneously throughout the pro-
cedure. Oxygen should be supplemented. There should be readi-
ness to convert to general anesthesia if the situation demands.
12.2. Asleep-awake-asleep (AAA) technique
This technique consists of general anesthesia before and after
brain mapping with or without involvement of an airway device at
the start and end of procedure. It consists of three phases. In the
first phase, patient is anesthetized. A laryngeal mask airway (LMA)
or an endotracheal tube (ETT) is used for ventilation. During phase
two, patient is aroused and the LMA or ETT is removed. Mapping is
executed when the patient is awake. During phase three, the pa-
tient is re-anesthetized and LMA or ETT is inserted after the map-
ping is over. LMA is most often used for the sleep phase due to its
ease of insertion, removal and re-insertion without changing the
position of patient and disrupting the surgical field [28,29]. ProSeal
LMA may be a better choice than classic LMA as the gastric tube
 A. Shetty et al. / International Journal of Surgery 36 (2016) 454e459
reduces the risk of gastric insufflation and pulmonary aspiration
[10]. I-gel can be used as an alternative to LMA [30].
12.3. Asleep-awake method
In this technique, scalp block is administered after induction of
anesthesia. Olsen et al. [31] used propofol and remifentanil infusion
and LMA during Asleep phase. After craniotomy is completed, pa-
tient is aroused and the LMA is removed. Nasal prongs can be
applied to administer oxygen.
Hansen et al. [32] described an awakeeawake technique. In this
technique, no sedation is required. Low dose opioid like remi-
fentanil may be required. They felt psychological support is more
useful than drugs.
13. Choice of anesthetic drugs for awake craniotomy
Choice of drugs depends upon whether functional cortical
mapping or electrocorticography is required. During awake crani-
otomy excess sedation may obtund airway reflexes. Sedation must
be just adequate to ensure comfortable and co-operative patient.
Sedation cannot compensate for inadequate block [33].
Regardless of the anesthesia technique, an adequate scalp block
is important for patient comfort as well as minimal disturbance in
cortical mapping and electrocorticography. Scalp block may be a
regional scalp block or a field block. In regional scalp block (Fig. 1),
the six nerves are blocked which includes: auriculo-temporal,
zygomatico-temporal, supraorbital, supratrochlear, greater occipi-
tal and lesser occipital nerves [34]. 2e3 ml of the drug is injected at
each point. In addition local anesthetic can be infiltrated at the
incision site. Epinephrine 1:200,000 dilution is added to reduce the
toxicity of local anesthetics and increase the duration of block [35].
The total amount of local anesthetic must be calculated for each
patient.
Field block involves LA infiltration along incision lines for the
scalp flap. Long acting drugs like bupivacaine, levobupivacaine and
ropivacaine are preferred. Costello et al. studied plasma concen-
tration of local anesthetics achieved after scalp block and they
found Ropivacaine (4.5 mg/kg) and levobupivacaine (2.5 mg/kg)
can be used safely [36,37].
Fig. 1. Scalp block for awake craniotomy. Numbers indicate the nerves to be blocked.1.
Supraorbital 2. Supratrochlear 3. Zygomaticotemporal 4. Auriculotemporal 5. Lesser
occipital 6. Greater occipital.
457
Neuroleptic-analgesia was used initially for awake craniotomy.
It consisted of fentanyl (0.5e0.75 mg/kg) and droperidol (0.15 mg/
kg). It had complications like prolonged sedation, seizures and risk
of prolonged QT interval [38]. Hence, it is replaced by propofol
because it is shorter acting, can be easily titrated and causes clear
headed recovery [39]. Other advantages include reduction in
intracranial pressure, anti-emetic and anti-convulsant effects. Pa-
tient controlled sedation using propofol, is an effective alternative
to neuroleptic-analgesia during awake craniotomy for epilepsy
surgery [40]. Intravenous anesthetic agents for awake craniotomies
include propofol, opioids (fentanyl and remifentanil) and
dexmedetomidine.
Propofol, with or without opioids is commonly used for awake
craniotomy. Herrick et al. [9] concluded that propofol infusion
should be stopped at least 15 min prior to ECoG monitoring for
optimal results. Target controlled infusion of propofol is preferred
over manual infusion for good titration and avoiding over sedation
[10].
The advantages of opioid based anesthesia are improved anal-
gesia and reduced requirement of other anesthetic agents. The
disadvantages are increased incidence of airway obstruction,
postoperative nausea, vomiting and seizures.
Gignac et al. [41] performed a study to compare analgesia,
sedation and the side effects of the newer opioids sufentanil and
alfentanil, with those of fentanyl in patients undergoing awake
craniotomy. Intravenous boluses of fentanyl: 0.75 mcg/kg sufenta-
nil: 0.075 mcg/kg, or alfentanil 7.5 mcg/kg followed by infusion
rates of 0.01 mcg/kg/min for fentanyl, 0.0015 mcg/kg/min for
sufentanil, 0.5 mcg/kg/min for alfentanil were used. They
concluded that the newer opioids did not offer any benefit over
fentanyl. Manninen et al. [42] did a comparison of continuous
remifentanil infusion (0.03e0.05 mcg/kg/min) with intermittent
fentanyl bolus (0.5e1 mcg/kg) in conjunction with propofol during
awake craniotomy for tumor resection. Both were found to have
similar patient satisfaction, recall and intraoperative complications,
although fewer patients experienced reversible respiratory
depression with the use of remifentanil. Therefore, all opioids are
equally good for use during awake craniotomy. Due to its short
duration of action and minimal effect on ECoG, remifentanil is a
good alternative for awake craniotomy as an adjuvant to other
drugs like propofol.
Dexmedetomidine has also been demonstrated to have minimal
effects on the electrocorticography and has been successfully used
in awake craniotomy for epileptic surgery. Doses can differ, but a
bolus of 0.3 mcg/kg with an infusion of 0.2 mcg/kg/hr has minimal
influence on monitoring, allowing accurate mapping of epileptic
foci and subsequent resection [11].
14. Complications of awake craniotomy [19,43]

Over sedation can cause apnea, hypoxemia, hypercapnia and
cerebral swelling.

Inadequate sedation may lead to hypertension, tachycardia and
patient discomfort.

Vomiting, shivering, LA toxicity, pain and poor patient co-
operation are also known complications of awake craniotomy.

Surgical complications may include seizures, aphasia, bleeding,
brain swelling and venous air embolism.
Hypotension occurred more commonly when propofol based
protocols were used, while nausea and seizures were more com-
mon when opioid based protocols were used. Respiratory compli-
cations were more common when opioids were combined with
propofol [18].
458 A. Shetty et al. / International Journal of Surgery 36 (2016) 454e459
15. Corpus callosotomy
There is a risk of uncontrolled hemorrhage and venous air em-
bolism during corpus callosotomy since the surgical approach is
near the sagittal sinus. Risk of aspiration pneumonitis and airway
obstruction in the immediate postoperative period is common in
these patients due to lethargy and somnolence [1].
16. Cerebral hemispherectomy (Functional)
Large craniectomy required for hemispherectomy can cause
massive blood loss and venous air embolism due to tearing of
venous sinuses. Complications of massive bleeding such as coa-
gulopathy, electrolyte and metabolic disturbances should be
anticipated. This procedure can be associated with seizures, cere-
bral edema, pulmonary edema and arrhythmias. In addition to non-
invasive monitoring, invasive blood pressure and central venous
pressure monitoring is required. Hemodynamic instability in the
postoperative period is common and thus elective postoperative
ventilation is advisable [1].
17. Vagal nerve stimulation (VNS) [44]
The placement of VNS requires general anesthesia and endo-
tracheal intubation due to its proximity to internal carotid artery
and jugular vein. Thus, large bore intravenous access should be
secured. Induction should be done taking into account the pro- and
anticonvulsant properties of anesthetic agents. Most of the cardiac
efferent fibers arise from the right vagus nerve and hence left side is
preferred for vagal nerve stimulator placement. VNS may be asso-
ciated with various types of arrhythmias especially bradyar-
rhythmias and asystole. ECG monitoring and resuscitative drugs
must be available perioperatively. Peritracheal hematoma and sei-
zures can occur in the postoperative period. Chronic vagal nerve
stimulation can lead to vocal cord paresis and risk of aspiration.
18. Conclusion
Anesthesia for epilepsy surgery must be tailored as per the
surgical requirement. The effects of anesthetic agents on ECoG and
cortical mapping and inherent risk of certain procedures must be
kept in mind.
Ethical approval
Not applicable.
Funding
None.
Author contribution
Dr. Anita Shetty e collected the information and helped in
writing the manuscript.
Dr. Swarada Pardeshi e helped in writing the manuscript.
Dr. Viraj M Shah e helped in writing and editing the manuscript.
Dr. Aarti Kulkarni e helped in writing the manuscript.
Conflict of interest statement
None.
Guarantor
Dr. Anita Shetty.
Research registration UIN
researchregistry174.
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