Anesthetic agents are proconvulsant or anticonvulsant.
Without exception,cerebral activity is affected in dose dependent manner with low doses activating the EEG,and large doses suppressing the activity.
This issue is very important during electro corticography (ECoG)when the interpretation of the tracing is critical in idetinfying the seizure focus.
Medication that alter EEG should be avoided if possible. Potent inhalational anesthesia which tend to be anticonvulsant have a depressine effect on the EEG at higher concentrations.
Halothane :
Produces progressive slowing of the EEG frequency.It also decreases sensory evoked potential(SEP) amplitudo in a dose dependent fashion.
It also increase visual evoked potential(VEP) latency and reduces amplitudo, Activation of epileptiform spikes is not seen. At concentration that are still clinically useful, suppression of the spike activity has been observed.
Enflurane :
Cause progressive slowing of the EEG and eventual burst depression. It can also reduce SEP amplitudo with slight effect on latency. Enflurane has been known to produce generalized seizures in patients with no previous history of seizure activity particularly in the presence of severe hypocarbia. Enflurane has been used as an activating agent
during diagnostic mapping at concentration of 2,5%.
Recently a synergistic role of enflurane and neuroleptic drugs in producing seizure activity has been confirmed.
Isoflurane :
Isoflurane decreases SEP amplitudo and high concentration, can completely suppress the scalp SEP.
Isoelectric EEG are noticed at levels in excess of 2 MAC.
Background epileptiform activity may be reduced or suppressed in the presence of low doses of isoflurane.
Most centers using low concentration of isoflurane simultanously with intravenous narcotic have not observed any negative effects. Elemination of N20 which potentiate the anesthetic effect of isoflurane and reduction of the inspired concentration to 0,25%(less than 2 MAC)
may minimize the suppressive effect.
Although isoflurane has intrinsically no proconvulsant effects,seizure activity has been reported in combination with N20.
Desflurane :
Produces EEG changes comperable to those observed with equipotent levels of isoflurane.No proconvulsant activity has been reported. Desflurane suppresses EEG activity significantly and burst suppression has been observed at 1,25 MAC and higher values.
Sevoflurane :
Increases in frequency and amplitudo of EEG tracing are observed with low concentration.At higher concentrations frequency and amplitudo decrease.No evidence of epileptiform activity has been observed.
Nitrous oxide:
Dose dependent EEG occur at N20 concentration above 25% N20 has no convulsant properties by itself, but in combina
tion with other agents potentiation has been noticed.
N20 can reduce the amplitude of auditory and visual evoked potentials with affecting the latency.
Cloor has claimed that N20 may negatively affect the inter
pretation of ECoG as it can suppress or eliminate spike activity.
Several centers will not use N20 during epilepsy surgery because of the suppressive effect on the ECoG.Others recommend discontinuation of N20 30 to 50 minutes prior to the recording of ECoG to avoid confounding interactions with other agents and to prevent whatever minimal effect
might be attributed directly to the agents.
Recent studies in non epileptic patients have indicated that combined with propofol,N20 will result in activation of
alpha and beta waves while on the other hand, depressed alpha and increased delta wave activity has been observed
in the presence of isoflurane.
Intravenous anesthetic agents:
Barbiturate :
Because of their many side effects most barbiturate no longer utilized as hypnotics and sedatives.
Barbiturate are traditionally anticonvulsant but may be avoided as bolus doses for treatment of seizure because of the rapid drug redistribution and subsequent reappearance of seizure activity. Contrary to the general trend all ultra
short barbiturate(thiopental,methohexital,amobarbital)
widely used in anesthesia.
Phenobarbital as a long acting component on the other hand is still prescribed for treatment of epileptic manifestation.
Barbiturate at low doses cause an increase in beta activity while higher doses successively produce EEG slowing and burst suppression and very high doses cause electrocortical silence.At low concentrations thiopental has proconvulsant properties and produces paroxysm of spike activity in epilep
tic patients.At higher doses it is potent anticonvulsant drug
Thiopental and pentobarbital have been widely used to treat postoperative seizures and status epilepticus.
Methohexital is a potent activator in patients with temporal lobe or primary generalized epilepsies. In low doses(as small as 25mg) activates the intraoperative cortical EEG and is at times used to unmask a seizure focus.
Amobarbital (in doses utilized for the Wada test) and methohexital has observed to produce spiking activation in the hipocampal region.
Propofol :
The effects of propofol on EEG are no different from intra
venous sedative hypnotic drugs;the agent induces dose dependent changes in the EEG.
The use of propofol is neither associated with cortical epileptic activity nor with aggrevation of esizures.
Patient with known and controlled epilepsy may receive propofol anesthesia. Moreover,propofol may be used to treat convulsion unresponsive to conventional treatment, this agents seems particularly useful for the inductions of coma therapy for controlling refractory epilepsy.
Like methohexital,propofol can increase epileptiform activity in patients known to have seizures.
Compared to barbiturates burst suppression is more easily controlled, awakening is more rapid and there are no hepatic side effects.
Ethomidate :
An ultrashort acting non barbiturate hypnotic agent with EEG changes similar to those of barbiturate.
In non epileptic patients myoclonic movement are common
ly observed, but this is not associated with any increase in epileptogenic activity on EEG. In epileptic patients,ethomi
date generates interictal spiking and at times initiated clinical seizures.
Ethomidate has been used to induce epileptiform activity during diagnostic ECoG. Wanquiter and et all,showed that using larger doses of ethomidate has strong anticonvulsant properties which could make it useful for treating refracto
ry status epilepticus.
Benzodiazepine:
Benzodiazepine are uniformly anticonvulsant through activa
tion of the inhibitory gamma amino butyric acid(GABA) channel and enhancement of chloride conductance.
Potent beta activators,are very efficaceous anticonvulsant should not be used when diagnostic ECoG is planned.
For presurgical invasive investigations for example,implan
tations of depth electrodes, midazolam may be utilized as part of a continuous infusion technique.
Ketamine:
The proconvulsant and anti convulsant properties of ketamine are dose dependent. Anti convulsant effects predominate at subanesthetic doses, whereas somewhat higher anesthetic doses are proconvulsant.
In non epileptic humans neuroexcitatory movements are common after the administration of ketamine. Opisthotonos and extensor spasm in infants and tonic clonic seizure in an adult have been reported following ketamine administration. However, EEG documentation of electrical seizure activity associated with ketamine is lacking in nonepileptic patients. Among epileptic patients ketamine reportedly activates epileptogenic foci. During ECoG seizure activity has been consistently demonstrated after the intra
venous administration of ketamine 2 to 4 mg/kg.
Opioids:
Various excitatory phenomena occasionally occur following the administration of opioids. Detailed studies using surface electrodes have failed to document any EEG,evidence of seizure activity in humans after fentanyl,alfentanil and sufentanil in high doses. On the other hand an incease
in delta activity arises after the rapid infusion of very large doses of sufentanil,with demonstrable ceiling effects.
The administration of fentanyl has resulted in a distinct seizure activity in deep temporal lobe structure of patients with complex partial seizures disorders;however no cortical seizure activity or motor activity was observed. Fentanyl,alfentanil,sufentanil have been compared one with another and found to be similar in their effects.
During anesthesia are used to produce analgesia and to reduce the demands for larger concentration of inhalation or intravenous agents. Patients chronically with AEDs (anti epileptic drugs) develops an increased tolerance to opioids and a typical doses-effect relationship has been demonstrated for fentanyl. Morphine does not appear to be associated with neuroexcitatory phenomena when adminis
tered intravenously at clinically appropriate doses.
In the operative setting doses of meperidine used in conjunc
tion with anesthesia do not appear to cause neuroexcitato
ry effect.
Dropridol:
Dropridol is frequently used in combination with fentanyl for providing neurolept analgesia during awake craniotomy.
In small doses it has a prolonged anti emetic effect. It has no effect on the EEG when given alone. At low doses in combination with fentanyl increased alpha activity is seen.
High doses cause high amplitude delta and beta activity.
In epileptic patients spike activity remains unchanged.
In combination with inhalation agents,neuroleptic agents appear to induce seizure activity.
Neuromuscular blocking agents:
They have no effect on the electrical central ctivity.
In anesthetized dogs,concntration of laudanocyne greater than 10 mcg/ml induced EEG epileptic spiking.The laudonocyne is the major end products of metabolism of atracurium.
In humans, no data substantiating a similar effect have been reported.Numerous studies have demonstrated major interactions between several AEDs and the musclerelaxant
Accelarated recovery has been observed with pancuronium,
doxacurium,vecuronium,pipericuronium and metocurine.
Atracurium appeared at first to be resistant for this action
but conflicting results have questioned the originally repor
ted effect. Succinylcholine has demonstrated opposite effects in patients on AEDs medication. In the presence of betamethasone,resistance to neuromuscular action of vecuronium was observed.
Local anesthetics:
They have biphasic effect on the EEG. At low plasma concentrations,lidocaine has anticonvulsant action.
At high concentrations,local anesthetic have excitatory effects and may induce seizures.
Larger than maximum recomended doses are frequently necessary for anesthetizing adequately the scalp and other sensitive structures.However few reports of toxic reactions have been published.
Possible explanation include the concomitant use of epinephrine with slows down systemic absorbtion,the phenytoin related increased detofication process and too low accepted plasma levels.
Low dose propofol have been recomended for treating lidocaine toxicity.
to be continued:
to be continued
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