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An extensive review of the convulsant and anticonvulsant effects of anesthetics and adjuvants is available.[409] [410] Several commonly used anesthetics have some epileptogenic potential, particularly in predisposed individuals. A concern is that seizure activity may go unrecognized in an anesthetized and paralyzed patient and result in neuronal injury if substrate demand (CMR) exceeds supply for a prolonged period.[411] A second concern is that the epileptogenic effect will persist in the postanesthesia period and seizures will occur in less well controlled circumstances than exist in the operating room. In practice, it appears that spontaneous seizures during or after anesthesia have been extremely rare events. Nonetheless, in patients with processes that might predispose to seizures, it seems prudent to avoid the use of potentially epileptogenic agents in situations in which reasonable alternatives are available.
The epileptogenic properties of enflurane and sevoflurane are discussed in the earlier section on volatile anesthetics.
Myoclonic activity is sometimes observed with methohexital, and this drug has been used to activate seizure foci during cortical mapping.[412] [413] One clinical report[414] describes the occurrence of seizures in two pediatric patients after induction doses of methohexital administered rectally in one and intramuscularly in the other. Both these patients had temporal lobe lesions and had previously had seizures. It appears that it is specifically patients with seizures of temporal lobe origin, typically of the psychomotor variety, who are at risk for activation of seizures by methohexital. [414] [415] Recurrent spontaneous seizures after methohexital anesthesia for ECT have never been reported.
Ketamine can elicit seizures in patients with an epileptic diathesis. [416] Depth electrode recordings in epileptic patients revealed the occurrence of isolated subcortical seizure activity originating in the limbic and thalamic areas during ketamine anesthesia and demonstrated that this subcortical activation may not be reflected in surface EEG recordings.[417] The occurrence of seizures after ketamine anesthesia in neurologically normal subjects has also been reported on only two occasions,[418] [419] and in one of these instances the seizure threshold may have been lowered by aminophylline.
Etomidate frequently produces myoclonus that is not associated with epileptiform activity on the EEG.[420] A single instance of severe, sustained myoclonus immediately after anesthesia with etomidate by infusion has been reported.[421] Etomidate has also been shown to precipitate generalized epileptic EEG activity in epileptic patients, [422] and its use in this population should probably be avoided. However, it has been used electively, in low doses, to activate seizure foci for the purposes of intraoperative EEG localization.[423] In our experience (unpublished), selective activation of a quiescent focus can be achieved with 0.1 mg/kg. Larger doses are more likely to lead to generalized activation.
Etomidate has also been noted to be associated with longer seizures in response to ECT than occur after methohexital or propofol. Remarkably, etomidate, in the dose range of 0.15 to 0.3 mg/kg, does not cause dose-related ECT seizure inhibition as is readily demonstrated with the other two agents.[424]
The preceding information not withstanding, no convincing reports have indicated that in normal subjects, epileptogenesis and the use of etomidate need to be restricted on this basis. In fact, etomidate has been used to control refractory status epilepticus.[425]
Seizures or limbic system hypermetabolism (or both) can be readily elicited in some animal species with narcotics.[211] [426] [427] [428] [429] Although an increase in CBF in deep brain structures associated with pain processing has been observed in human volunteers, [208] humans do not have a clinically apparent correlate of the hypermetabolism effect seen in animals. Several anecdotal reports, unaccompanied by EEG recordings, maintain that grand mal convulsions have occurred in patients who received both high[430] and low doses of fentanyl. [431] [432] However, systematic investigations of EEG changes during the administration of relatively large doses of fentanyl, sufentanil, and alfentanil in humans have not documented neuroexcitatory activity,[433] [434] [435] and the "seizures" may have been an exaggerated rigidity phenomenon. The exception is the observation that alfentanil, 50 µg/kg, can augment temporal lobe spike activity in patients with temporal lobe epilepsy. [436] Note that untreated rigidity may itself also have important CNS consequences. An increase in ICP was observed when alfentanil-induced rigidity occurred in rats during controlled ventilation.[381] The effect probably arose because the associated increase in CVP caused cerebral venous congestion. In the absence of ventilatory support, both hypercapnia and hypoxemia may also occur.
See the discussion regarding the atracurium metabolite laudanosine in the section on nondepolarizing muscle relaxants.
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