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Epilepsy surgery

The term ‘epilepsy surgery’ refers to:

intra-op

The core principles of neuroanaesthesia include:

Nitrous oxide increases cerebral blood volume and possibly cerebral metabolic rate (CMR) and is best avoided

The relationship between inhalation anaesthetic agents and cerebral blood flow is complex, and in most cases an increase in cerebral blood volume is offset by a decrease in CMR.

It is a common practice in neuroanaesthesia to use sevoflurane or isoflurane to a level of 1 MAC with a remifentanil infusion for maintenance of anaesthesia

Long-term administration of AED is associated with resistance to NMBA

Some patients may be following a ketogenic diet, in which case the use of normal saline solutions is preferable to lactated Ringer's solution

Key moments

Head clamp, Mayfield pins: very stimulating

Intra-op electrocorticography (ECoG)

EEG electrodes are placed directly on the cortical surface and epileptiform activity is identified, and this can guide the extent of a resection

As the intraoperative time is short, clinical seizures are usually not captured by ECoG, but the presence and location of IEAs (interictal epileptiform activities) can be used to localise the epileptogenic focus and guide the resection

If ECoG is required, then benzodiazepines should not be given on induction because they suppress EEG activity

During ECoG, pharmacoactivation may be required in order to activate IEAs. Potent short-acting μ-agonists can be used to increase IEAs and alfentanil, remifentanil, fentanyl and sufentanil can be used for this

It is generally accepted that the depth of anaesthesia should be reduced during ECoG, and the patient should be advised of the small risk of awareness during this period

Neuromuscular blockade may be used to prevent movement and interference with ECOG; it should be noted that laudanosine, a metabolite of atracurium and cisatracurium, is potentially epileptogenic

Activates IEAs Suppresses IEAs Variable IEA effect Background ECoG
Intravenous anaesthetics Thiopental—activation with boluses

Etomidate—may provoke seizures

Ketamine—non-specific activation

Methohexital—significant activation of spikes		 Benzodiazepines Propofol—may activate or suppress spikes with variable effect over all dose ranges

Dexmedetomidine—no evidence of activation or suppression		 An initial desynchronisation is seen followed by progression into β, θ and δ waves and subsequent burst suppression.
Benzodiazepines and dexmedetomidine have a similar spectral profile.
Inhalation anaesthetics Sevoflurane—non-specific dose-dependent activation

Enflurane—may provoke seizure particularly if Paco2 low		 Halothane
Nitrous oxide—suppresses at concentrations >50% and acts synergistically with other agents		 Desflurane—no evidence of activation

Isoflurane—may suppress spikes especially if used with nitrous oxide

Xenon—effect unclear but likely does not cause activation		 Burst suppression achieved at concentrations >1.5 MAC
Opioids Fentanyl, alfentanil, remifentanil, sufentanil—all cause activation at high doses and potentially at common clinical doses

Pethidine—probably causes activation		 Morphine, hydromorphone—likely no effect at clinical doses but potentially at high doses Low-dose infusions have no effect on background ECoG

IOM
Direct cortical stimulation with motor mapping is associated with an increased risk of seizures compared to transcranial electrical stimulation alone.

Awake craniotomy

There are two main advantages of resection of epileptogenic foci in the awake patient.

Firstly, for lesions in eloquent areas of speech and sensorimotor function, surgery in the awake patient allows for continuous monitoring of these functions, that is language and sensorimotor mapping, to guide the extent of the resection.

Secondly, ECoG can be performed without the interference of anaesthetic agents.

Disadvantages include

Awake craniotomies require a calm and cooperative patient and are often not feasible in children, those with intellectual disabilities or a significant psychiatric history

Intra-op seizures

If pharmacoactivation during ECoG or cortical electrical stimulation for functional mapping is required, the patient may develop seizures. These are usually focal seizures that cease when stimulation has stopped, but they may progress to generalised tonic–clonic seizures.

The first step in management is to irrigate the surgical field with ice cold saline.

If this manoeuvre fails, then propofol boluses of 10–30 mg should be administered.

Subsequently benzodiazepines (midazolam 2–5 mg) or thiopental (25–50 mg) can be used if the seizure is ongoing.

Management of intraoperative seizures should be in conjunction with the neurophysiologist given that any drug administered for the termination of seizures may affect subsequent ECoG monitoring.

In cases where ECoG is not being used, the detection of seizures is challenging.

Younger age, recent seizure activity, frontal and parietal lesions and certain tumours such as oligodendrogliomas are all associated with an increased risk of developing intraoperative seizures

Hypocapnia can also provoke seizure activity and should be avoided

Clinical signs include

Fluctuations in bispectral index (BIS) are observed with intraoperative seizures, generally seen as a decrease in BIS level followed by an increase.

Reports of BIS changes with seizures are inconsistent and in the context of epilepsy surgery can be misleading. If there is a concern regarding seizure activity in the absence of EEG monitoring, the depth of anaesthesia should be increased and a benzodiazepine administered.

Post-op

Delayed emergence is common in patients after epilepsy surgery for several reasons:

Some patients with an ‘irritable’ EEG may require loading doses of AEDs during surgery after recording, or after operation.

Administration of large doses of opioids should be avoided and in the absence of large blood loss or other contraindications non-steroidal anti-inflammatory drugs can be given.

Seizures and the postictal state may cloud neurological assessment and early detection of new haemorrhage

For generalised tonic–clonic seizures occurring in the PACU, benzodiazepines are first-line therapy

Given that seizure activity causes an increase in lactate, the lactate level should not be used in isolation to guide fluid management or as a criterion for discharge from the PACU

It is important that doses of AED are not missed after surgery. Given that many AEDs cause hepatic enzyme induction or inhibition, the different interactions should be considered

Enzyme-inducing drugs ↓ the serum concentrations of many drugs including paracetamol, fentanyl and some antibiotics
enzyme-inhibiting drugs may ↑ serum concentrations of antibiotics and in particular other AEDs

The risk of blood loss is increased with second and subsequent craniotomies.

References

Epilepsy and Anaesthesia

Epilepsy Advanced Anesthesia Review Oxford Academic

Adult Epilepsy and Anaesthesia

Anaesthesia and Epilepsy

Anesthetic Management of the Patient With Epilepsy or Prior Seizures