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Anesthetic Considerations for Awake Craniotomy for Epilepsy ... - Vtr

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254<br />

Erickson & Cole<br />

Medications<br />

Several specific medication effects have been studied with regard to awake craniotomy<br />

<strong>for</strong> epilepsy and functional neurosurgery.<br />

Propofol, although providing good patient satisfaction and antiemetic and antiepileptic<br />

effects, may cause oversedation and poor operating conditions. Propofol is<br />

associated with hypoventilation, although this is less of a problem when a targetcontrolled<br />

infusion is used or when opioids are not added. 114,134 During DBS insertion,<br />

less propofol may be required in patients with Parkinson disease than is predicted by<br />

target-controlled infusion models. 167<br />

Opioid-based techniques are associated with increased reports of seizures and<br />

nausea. 142 Among opioids, none of the short-acting fentanyl congeners, including<br />

the ultra–short-acting remifentanil and alfentanil, used <strong>for</strong> awake craniotomy has<br />

been shown to be superior to its peers. Comparisons of fentanyl with sufentanil and<br />

alfentanil, and remifentanil with fentanyl, do not show any differences in complications<br />

and all provided good clinical conditions although a case report described severe<br />

remifentanil-induced opioid tolerance in a 16 year old. 118,142,168 The desirable brevity<br />

of action common to these opioids may require the use of a longer-acting opioid <strong>for</strong><br />

postoperative pain control. 168 The problems of respiratory depression and increased<br />

brain volume (discussed previously) as well as airway obstruction and desaturation are<br />

common to all opioids.<br />

Dexmedetomidine, the selective a2-agonist, has been used <strong>for</strong> both MAC and AAA<br />

management of awake craniotomy and DBS implantation since the first case report<br />

by Bekker and colleagues in 2001. 141,150,151,154,161–166,169 The successful use of dexmedetomidine<br />

has even been reported in children as young as 12 years. 163,166 Dexmedetomidine<br />

provides analgesia with minimal respiratory depression (little risk of<br />

hypercapnea), cooperative sedation, anxiolysis without agitation or hangover effect,<br />

and hemodynamic stability. Lower doses are suggested <strong>for</strong> awake craniotomy,<br />

because higher doses can impair patient responsiveness. 170 It may be used alone <strong>for</strong><br />

sedation and analgesia, or with volatile, nitrous oxide, or total intravenous anesthesia<br />

as an adjunct to smooth induction, and emergence. Dexmedetomidine alone may be<br />

ideal <strong>for</strong> DBS implantation because it does not depend on GABAergic pharmacology<br />

and also does not suppress target symptoms, such as tremor or dyskinesia. 137,153,154<br />

High-dose dexmedetomidine, however, has been shown to interfere with MERs. 137<br />

Likewise, Oda and colleagues 152 reported changes in ECoG recordings during epilepsy<br />

surgery with dexmedetomidine use at higher doses (discussed previously). The main<br />

disadvantages of dexmedetomidine include hypotension and bradycardia, which are<br />

reported to be dose related and treatable, if not preventable. 171<br />

<strong>Anesthetic</strong>s and Microelectrode Recordings<br />

One of the main purposes of the awake state <strong>for</strong> DBS placement is to avoid interference<br />

of general anesthesia with MERs from deep brain structures.<br />

Benzodiazepines seem to abolish MERs and may induce dyskinesias. 103,128,172<br />

Although there are no prospective data, it seems that anesthetics do not uni<strong>for</strong>mly<br />

depress MERs but rather differ by disease as well as by deep brain site/nuclei. For<br />

example, desflurane seems to depress MERs from the globus pallidus internus (GPi)<br />

in Parkinson disease but not in dystonia. 173 Reports of GPi recordings, both unaffected<br />

and depressed by propofol, have been published. 135–137,154,174–176<br />

In contrast, MERs from the subthalamic nucleus (STN) seem relatively more robust<br />

under anesthesia, which has been attributed to its lower GABA input compared with<br />

the GPi. 177 Benzodiazepines seem to abolish MERs and may induce dyskinesias. 172

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