Hi Emma3094-ga, and thanks for your question. My condolences if you
or a loved one is afflicted with a new onset seizure disorder. A good
friend of mine struggled with seizures for most of her life. As
usual, the following is not a substitute for medical advice or direct
The references for the information provided below are grouped at the
end of the answer and are referenced within the answer using brackets
[Ref #]. Because the references I've used are not freely available,
I have provided relevant quotations from them. Where applicable, I
have also included the e-mail addresses of the corresponding authors,
from whom you can request free reprints of their articles. Authors
are usually happy to do this, and can often simply e-mail you a PDF of
The type of surgery can obviously play a role in the development of
post-operative seizures, irrespective of the type of anesthesia used.
For example, resection of brain tumor in the temporal lobe can result
in post-operative seizure disorder. As you ask specifically about
general anesthesia induced seizures, I will focus on this topic.
Miller's Anesthesia [Ref #9], one of the major textbooks of
anesthesiology and a valuable resource on this topic, discusses at
various points the topic of various anesthesia agents and seizures. I
have collected the relevant quotes from this text below for various
anesthesia agents and anesthesia-related drugs below:
Enflurane ([Ref #9], page 829):
"Enflurane is potentially epileptogenic in the clinical setting. Of
particular relevance to neuroanesthesia is the observation that
hypocapnia potentates seizure-type discharges during enflurane
anesthesia. A 50% decrease in CMRO2 was noted in human
volunteers anesthetized with 3% enflurane, but with the onset of
seizure activity, CMRO2 returned to normal, thus indicating
preservation of flow-metabolism coupling. Note that there is no
evidence that this type of EEG activity is deleterious when oxygen
delivery is maintained during the event. However, because seizure
activity can elevate brain metabolism by as much as 400%, the use of
enflurane, especially in high doses and with hypocapnia, should
probably be avoided in patients who are predisposed to seizures or
have occlusive cerebrovascular disease.
The EEG-activating property of enflurane has been used
intraoperatively to activate and identify seizure foci that are to be
surgically resected, and in this situation, spike activity not present
preoperatively has been observed to persist after surgery. In
addition, two reports have described seizures in the immediate
postoperative period after enflurane anesthesia in both
predisposed and nonpredisposed individuals.  No apparent
permanent sequelae have resulted from these events, and in fact, this
association is not a rigorously proven one. At worst, such
occurrences are extremely uncommon."
Isoflurane ([Ref #9], page 829):
"Isoflurane can cause EEG spiking and myoclonus, but in the
experimental setting it has not been associated with the frank
epileptoid activity induced by enflurane. The clinical experience with
isoflurane is very large, and unexplained "seizure-like activity" has
been reported in only two patients. One incident occurred
intraoperatively  and the other immediately postoperatively.
 It therefore appears that epileptogenesis is not a clinical
concern with isoflurane. In fact, isoflurane has been successfully
used to control EEG seizure activity in refractory status
Sevoflurane ([Ref #9, page 830):
"Seizures have been reported to occur during induction of anesthesia
with high concentrations of sevoflurane in children, including those
without a recognized seizure diathesis.  In two healthy
human subjects, EEG burst suppression with 2 MAC sevoflurane was
accompanied by epileptiform discharges that were observed during EEG
monitoring.  These discharges were associated with a significant
increase in CBF, thus demonstrating that flow and metabolism coupling
was preserved. In patients with temporal lobe epilepsy, the
administration of 1.5 MAC sevoflurane elicited widespread paroxysmal
interictal EEG activity. Of note was the observation that paroxysmal
activity was not restricted to the ictal focus and that the
administration of sevoflurane was not of any assistance in
localization of the epileptogenic region of the brain. The
development of tonic-clonic movements indicative of seizure activity
has also been reported in otherwise healthy patients on emergence from
sevoflurane anesthesia.  In all of the reported cases of
seizure activity associated with sevoflurane anesthesia, untoward
sequelae have not been documented. These reports highlight
sevoflurane's ability, albeit small, to evoke epileptiform activity,
and accordingly, the use of sevoflurane in patients with epilepsy
should be undertaken with appropriate caution.
Laudanosine (a breakdown product of atracurium, used as a paralysis
agent during the induction of anesthesia):
"A metabolite of atracurium, laudanosine, may be epileptogenic.
However, although large doses of atracurium caused an EEG arousal
pattern in dogs, CBF, CMR, and ICP were unaltered. In cats, the
seizure threshold for lidocaine-induced seizures was not different
during paralysis with atracurium, vecuronium, or pancuronium. In
rabbits, administration of laudanosine did not increase the severity
of the epileptoid activity caused by direct application of
cephalosporin to the cortical surface. It appears highly
unlikely that epileptogenesis will occur in humans with atracurium.
There have been a handful of cases of seizure disorders resulting from
general anesthesia in the published medical literature. Drs. Akeson
and Didriksson [Ref #1] reviewed cases of seizures in two young
children felt to be associated with the use of sevofluorane.
Here is their summary of these cases:
"Case 1: during induction of anaesthesia with sevoflurane by facemask
in a 3-year-old healthy boy, there were symmetrical clonic
seizure-like movements of the upper extremities for 60 s..."
"Case 2: on re-induction of anaesthesia with sevoflurane because of
profuse bleeding following nasal adenoidectomy in a 4-year-old healthy
girl with a family history of epilepsy, there were symmetrical tonic
and clonic seizure-like movements for 3040 s in the upper and lower
extremities. Both episodes ceased spontaneously..."
Here is a more detailed account of these two cases from the text of
their paper, which includes details on what medications were used,
"During the induction of anaesthesia with sevoflurane by facemask in a
3-year-old healthy boy, symmetrical clonic seizure-like movements of
the upper extremities were observed. These movements lasted for 60 s
and ceased spontaneously.
A 3-year-old healthy boy weighing 17 kg with no previous experience of
anaesthesia was scheduled for abrasion of the nasal adenoid. He had
never had seizures, nor did he have a family history of epilepsy.
Twenty minutes before anaesthesia was induced, the child was given
midazolam 5.1 mg, paracetamol 250 mg and atropine 0.34 mg rectally for
premedication. He was well sedated on arrival in the operating room.
The boy was subjected to preoxygenation via facemask for 23 min and
was then exposed to gradually increased concentrations (range 0.56%)
of sevoflurane in oxygen 2.5 l min1 and nitrous oxide (N2O) 2.5 l min1
provided via a rebreathing anaesthesia circuit equipped with a Penlon
vaporiser (Penlon Ltd, UK) and a sodalime CO2 absorber.
After 34 min, when the patient was clinically anaesthetized (parallel
and centralized eye axes, medium-sized pupils) at an expiratory
sevoflurane concentration of 3%, as well as adequately oxygenated
(SpO2 99%) and ventilated (endtidal CO2 4.7 kPa), there were sudden
symmetrical regular slow clonic movements of both upper extremities.
The N2O was immediately exchanged for oxygen, and a teflon cannula was
rapidly inserted in a dorsal hand vein, but by that time the movements
had stopped spontaneously. The episode of convulsions lasted
approximately 60 s, and during this period the heart rate decreased to
100 min1 from 130 min1 immediately after the end of induction.
After this point, anaesthesia was uneventful. The patient had 30 µg of
fentanyl and 30 mg of suxamethonium administered intravenously (i.v.),
and an oral endotracheal tube was inserted. After intubation the
sevoflurane was exchanged for isoflurane to maintain further
Surgery was carried out as planned, and there were no problems during
emergence from anaesthesia or later in the postoperative period."
"A 4-year-old healthy girl with a family history of epilepsy had
undergone uneventful nasal adenoidectomy under general anaesthesia
with sevoflurane. On emergence from anaesthesia there was sudden
profuse bleeding from the nose. During re-induction of anaesthesia
with sevoflurane via the endotracheal tube there were tonic and slow
clonic seizure-like movements for 3040 s in the upper and lower
A girl aged 4 years and weighing 14 kg was scheduled for abrasion of
the nasal adenoids and bilateral tympanic paracenthesis. She had no
previous history of epilepsy, but her mother and elder sister were
both reported to be epileptics.
Approximately 20 min before induction of anaesthesia, the girl was
given midazolam 4.2 mg, paracetamol 250 mg and atropine 028 mg
rectally for premedication. She was adequately sedated when brought to
the operating room.
The girl was preoxygenated by facemask for approximately 2 min. She
was then given increasing inspiratory concentrations (0.56%) of
sevoflurane in oxygen 3 l min1 and N2O 3 l min1. Approximately 4 min
later, the patient had centralized, parallel eye-axes and medium-sized
pupils at an endtidal sevoflurane concentration of 3.03.2%, and was
adequately oxygenated (SpO2 99%) and ventilated (endtidal CO2 4.54.7
kPa). The N2O was then exchanged for oxygen. A dorsal hand vein was
cannulated and 0.15 mg of atropine together with 20 mg of
suxamethonium and 30 µg of fentanyl were given i.v. Oral endotracheal
intubation was carried out, and anaesthesia was then maintained with
sevoflurane in an even 1 l min1 mixture of oxygen and N2O.
On emergence from anaesthesia, after the supplies of N2O and
sevoflurane had been turned off for several minutes and the patient
had regained control of her gag reflex, there was sudden profound
nasal bleeding calling for rapid surgical re-intervention.
Anaesthesia was rapidly re-induced by controlled ventilation via the
endotracheal tube with up to 8% (vaporiser setting) sevoflurane in an
even 6 l min1 mixture of oxygen and N2O. After approximately 90 s,
when a sinus tachycardia of 160 min1 had just appeared, tonic
generalized convulsions were observed for 510 s and immediately
followed by symmetrical, regular, slow, clonic movements of the upper
and lower extremities. The sevoflurane and the N2O were both turned
off and pure oxygen supplied, and roughly 30 s later the convulsions
disappeared. By then the heart rate was 130 min1. Throughout this
episode the SpO2 was 9799% endtidal CO2 at an 4.64.8 kPa. Thiopentone
75 mg i.v. was administered and isoflurane in pure oxygen was used to
maintain further anaesthesia while the bleeding was stopped
successfully. Emergence from anaesthesia was uneventful, and so was
the further postoperative course."
The authors [Ref #1] go on to put these cases in historical context,
with regards to prior experience with sevofluorane:
"Since commercial release of sevoflurane on the global market in 1990,
there have been several clinical reports of tonic and clonic
seizure-like movements in patients undergoing sevoflurane anaesthesia
(14). Some authors (313) have even suggested a correlation between the
exposure to sevoflurane and electrocortical seizure activity."
The authors [Ref #1] also discuss other anesthesia agents with regards to seizures:
"Epileptiform EEG activity in nonepileptic patients has been found to
be associated with the use of sevoflurane for induction of anaesthesia
in children (12) and adults (10, 11, 13) as well as for maintenance of
anaesthesia in adults (3, 6). In contrast, no EEG seizure activity was
found in patients also given midazolam (14), thiopental (15) or
fentanyl (16), and nitrous oxide has accordingly been reported to
attenuate (9) or to have no effect on (4) the EEG response to
sevoflurane. Apart from the sevoflurane, the only drugs possibly
associated with the seizure-like activity in our patients were
midazolam, fentanyl and N2O. Based on findings by others (4, 9, 14,
16) we propose that the administration of these drugs together with
sevoflurane would rather have attenuated than facilitated clinical
convulsions similar to those found in our patients."
Another very recent paper [Ref #2] explored the potential for
sevoflurane to cause seizures in children without a history of seizure
Table 1 of this reference [Ref #2], too bulky to reproduce here, gives
an up to date listing of all studies that have looked at seizures and
sevoflurane, most of which are case reports and small studies. None
of the studies demonstrated prolonged seizure activity of the type you
describe after anesthesia. Most of the epileptigenic effects of
sevoflurane appear to be clinically important during induction (when
the patient goes to sleep). This is also the case with [Ref #1],
where seizure-like movements were observed at the induction of
anesthesia, but not after recovery.
The observation of seizures or seizure-like activity in all of these
studies varied quite a bit, as [Ref #2] points out:
"For example, under steady-state conditions in adults, Jaaskelainen et
al. and Sato et al. found seizure-like activity in all patients at
>1.5 MAC sevoflurane in 100% O2 (6,8), while Iijima et al. found none
under similar conditions (9). During sevoflurane induction (8% in
O2-N2O, 50 : 50) in children, Vakkuri et al. described minimal (minor)
seizure-like activity in 80% (10), while our team found none during
similar conditions of induction (11). Apparently the observation of
minor epileptiform changes may be tied to the neurophysiologist
observer, the major epileptoid signs such as periodic discharge,
epileptiform discharge, or frank seizure activity seem to be more
The means by which sevoflurane may help induce seizures is unknown.
Here is the best current hypothesis [Ref #2]:
"The mechanism of the epileptogenic effect of sevoflurane is thus far
unknown. The hypothesis that it resembles that of enflurane (biphasic
and dose-dependent activation of NMDA neuronal receptors) is supported
by similarity in molecular structure, but remains to be proved."
The authors [Ref #2] state that no permanent seizure disorders have
been attributed to sevoflurane, but that further work is needed:
"No neurological sequelae such as seizure have been thus far
attributed to the use of sevoflurane. However, until now no study
looking at the persistence or emergence of epileptiform EEG activity
on follow-up has been published and further research in this area is
required. However, in view of the tens of millions of sevoflurane
anesthetics given worldwide, concern about epileptogenic potential of
sevoflurane is expected to be minimal. This perspective is further
justified by the excellent cardiovascular stability preserved during
sevoflurane inhalation induction."
[Ref #2] also points out that seizures with and after anesthesia can
be due to coincidental brain pathology, having nothing to do with the
"One case of seizure has been reported in a 19-year old with a
cerebral cortical lesion but no prior convulsion, who experienced a
generalized tonic-clonic seizure during emergence from sevoflurane
This patient had a mass lesion within his brain causing seizures,
which happened to be revealed during anesthesia (not because of it).
At times of physiological stress, the brain is more prone to seizures.
This is why the most sensitive EEG studies are performed when the
patient is sleep deprived - the seizures are more likely to occur so
that they can be captured on EEG.
Your description is concerning in that you state that the seizures
last 4-5 hours. Seizures lasting greater than 30 minutes (some say as
little as 4-5 minutes) are considered status epilepticus, a serious,
life threatening (20% mortality) condition that can result in
permanent neurological damage. If seizures cannot be controlled at
this time point, coma is often induced to protect the brain and body
from further damage.
The American Association of Family Physicians (AAFP) has a very good
protocol for the management of Status Epilepticus:
eMedicine, another excellent resource, has a page on status
epilepticus primary from an adult standpoint:
A second eMedicine page discusses status epilepticus in children:
Given the rarity of anesthesia associated seizures, particularly the
prolonged type you describe, one must entertain the possibility that
something else is going on here. I alluded to one possibility earlier
- the seizures could be unrelated to the anesthesia and/or to the
surgery, and were coincidentally unmasked. In the absence of some
type of head trauma, this is an unlikely, but not impossible
There have been reports of pseudoseizures in patients after general
anesthesia. Pseudoseizures are a complicated topic and are
categorized as somataform disorders. Many clinicians believe that
this categorization means that the seizures are "faked" or "all in the
head." This does not appear to be the case and, for this reason, some
newer literature refers to pseudoseizures as "non-epileptic seizures
(NES)." Their etiology is complex and not understood. While there
does appear to be a psychological component, this isn't the whole
story. The diagnosis of pseudoseizures can be made by obtaining a
normal EEG during a epileptiform episode. Sometimes this is done
using video monitoring (patient stays in the hospital under
surveillance with electrodes on the head for the EEG). When an
episode occurs, the EEG for that time period is analyzed for seizure
activity. Absence of EEG changes typical of seizure activity bumps
the patient into the pseudoseizure category.
Here are some reports of this type of this type of disorder after
The authors of [Ref #3] cite two patients two developed pseudoseizures
after general anesthesia for benign procedures (MRI and vaginal
delivery with subsequent sedation). My own opinion is that this
particular case is more likely to represent an atypical case of
eclampsia (seizures during delivery following severe hypertension)
than pseudoseizure. For more details, see, for example, page 2329 of
The authors of [Ref #4] cite another patient, who had a known seizure
disorder, who developed pseudoseizure disorder following general
"A 47-yr-old woman underwent general anaesthesia for a squint
correction. She had previously suffered a cerebral venous thrombosis,
presenting as grand mal seizures during recovery from general
anaesthesia for minor surgery. Subsequently, she was affected by
Jacksonian limb seizures and petit mal epilepsy and had required
long-term rehabilitation, and anticonvulsant and anticoagulant
therapy. On arrival in recovery on this occasion, with a laryngeal
mask airway (LMA) in place, she started to convulse. The seizures were
initially treated with midazolam i.v., but they recurred. Whilst
observing the seizure pattern and excluding the differential
diagnoses, evidence emerged that psychological factors had played a
large part in her clinical picture. Her differential diagnosis had
recently been amended to include 'pseudoseizures'. A firm, supportive
approach caused the 'convulsions' to cease within a few hours."
This leads to the question, Can there be "psuedostatus epilepticus?"
This entity is not well described in the medical literature, but some
authors have looked into it.
A group in Germany [Ref #5] describes a 9-year-old child with
epilepsy, who presented with what appeared to be status epilepticus.
Here is the abstract from their article:
"Pseudostatus epilepticus in childhood has not been well reported in
the literature. We describe the clinical presentation and management
of a 9-year-old child with well-controlled epilepsy who presented in a
prolonged period of pseudoseizures. Intensive care management over a
number of weeks with multiple high-dose antiepileptic drugs,
anesthesia, and ventilation at a tertiary care pediatric center was
performed before the diagnosis of pseudostatus epilepticus was made.
Initiation of family counseling and behavior therapy after diagnosis
of the nonepileptic nature of the protracted paroxysmal events with
video telemetry in our pediatric epilepsy unit was followed by
remission. The patient reported herein illustrates the risks of
iatrogenic morbidity that may result from a delay in the diagnosis of
pseudoseizures and pseudostatus epilepticus in childhood."
A second group from the UK [Ref #6] describe 13 patients with
pseudostatus epilepticus, whom they compare to 13 matched patients who
presented with confirmed (genuine) status epilepticus:
"Thirteen patients with pseudostatus (simulated status epilepticus)
have been compared to 13 patients with true status epilepticus seen at
a regional neurological centre. Pseudostatus was common in patients
with pseudoseizures and was often misdiagnosed as status epilepticus.
Complications of this misdiagnosis included eight episodes of
anticonvulsant-induced respiratory arrest. Patients with pseudostatus
commonly had multiple episodes of 'status'. They usually also had a
history of other unexplained illness and of deliberate self-poisoning.
Management of these patients was difficult and emphasizes the need for
specialist expertise for patients with epilepsy and apparent
One interesting paper from a group in the UK [Ref #7] recently looked
at withdrawing antiepileptic medications in patients with
pseudoseizures. Here is their abstract:
"BACKGROUND: To determine whether withdrawal of anticonvulsant
medication (AED) can be carried out safely in patients with
non-epileptic seizures (NES, pseudoseizures). METHODS: Prospective
evaluation of safety and outcome in 78 patients with NES who satisfied
a standardised set of criteria for excuding concomitant epilepsy.
Findings: The patients were taking from 1-3 AED. Sixty four patients
were withdrawn as outpatients, 14 as inpatients. Five patients stopped
their medication abruptly, and two had AED restarted, and had to be
withdrawn again. Otherwise all patients adhered to withdrawal
schedules. A new type of attack as well as NES was seen in 3 patients,
in all 3 cases complex partial seizures. NES frequency declined in the
group as a whole over the period of the study (follow up 6-12 months)
in all individuals except for 8 patients in whom there was a transient
increase. Fourteen patients reported new physical symptoms after
withdrawal however no serious adverse events were reported.
Interpretation: With appropriate diagnostic investigation and
surveillance during follow up withdrawal of AED can be achieved safely
in patients with NES."
Finally, one article [Ref #8] puts all of this into perspective from
the point of view of the anesthesiologist, discussing peri- and
post-anesthesia pseudoseizures. The paper discusses signs suspicious
for pseudoseizures for the anesthesiologist or other clinician:
"Postoperative epileptic seizures are recognised but rare. Psychogenic
seizures and pseudostatus epilepticus are relatively common,
particularly in the peri-operative period. Our series of five cases of
postoperative pseudostatus epilepticus demonstrates that the failure
to recognise the psychogenic nature of this condition may cause
anaesthetists to give inappropriate and potentially harmful treatment.
Psychogenic 'status' is easy to diagnose once it has been considered.
Convulsive episodes lasting longer than 90 s, closed eyes during a
'tonic-clonic' attack, retained pupillary response and resistance to
eye opening are useful signs. Often there is a history of multiple
admissions with 'status epilepticus' and of previous postoperative
Another possibility, although you don't mention it in your question,
is anoxic brain injury during surgery. If, for some reason, the
oxygen supply to the brain was interrupted or sufficiently diminished,
anoxic brain damage can occur, resulting in epilepsy.
Seizure disorders are much better treated today than in the past.
Medical therapy is the first line approach. For patients with
seizures that are refractory to medical therapy, if there is a focal
region of the brain generating epileptigenic signals (and this area
can be resecte safely), functional neurosurgeons can remove the
offending portion of the brain, usually the temporal lobe, often with
amazing results. My friend had this type of surgery and has been
seizure free now for about 10 years - after having up to 20 seizures
Here is an article on epilepsy and seizure disorders, including a good
summary of treatments available:
eMedicine also has a good article discussing pseudoseizures with a
very good discussion of diagnosis and treatment.
Both of these articles have complete bibliographies if you should want
to pursue these topics further.
This is a lot of information, so let me summarize... While some agents
used in anesthesia can cause seizures, there is essentially no good
evidence that any of these agents by themselves cause long term
seizure disorders. There is some literature to suggest that
pseudoseizures (also known as non epileptic seizures) can arise after
surgery and general anesthesia. Their etiology is complex and not
understood. Seizures lasting more than 30 minutes (some say 5
minutes) are termed status epilepticus and are an emergency. There is
an entity known as pseudostatus epilepticus, which is a pseudoseizure
that lasts more than 5-30 minutes. There are many treatments for
seizures, ranging from medical to surgical treatment, or psychiatric
and medical modalities for pseudoseizures.
I hope this information was useful. Please feel free to ask for any clarification.
Akeson J., Didriksson I. Convulsions on anaesthetic induction with
sevoflurane in young children. Acta Anaesthesiologica Scandinavica,
Volume 48 Issue 4 Page 405 - April 2004.
You can request a full text reprint of this article from Dr. Akeson at
Constant I, Seeman R, Murat I. Sevoflurane and epileptiform EEG
changes. Pediatric Anesthesia, Volume 15, Issue 4, Page 266 - April
You can request a full text reprint of this article from Dr. Constant
at this address:
Allen G, Farling P. Anaesthesia and pseudoseizures. Br J Anaesth.
The full text is available free from this link:
Ng L, Chambers N. Postoperative pseudoepileptic seizures in a known
epileptic: complications in recovery. Br J Anaesth. 2003
The full text is available free from this link:
Tuxhorn IE, Fischbach HS. Pseudostatus epilepticus in childhood.
Pediatr Neurol. 2002 Nov;27(5):407-9.
Abstract is here:
Howell SJ, Owen L, Chadwick DW. Pseudostatus epilepticus. Q J Med.
Abstract can be found here:
Oto M, Espie C, Pelosi A, Selkirk M, Duncan R. Safety of
antiepileptic drug withdrawal in patients with non-epileptic seizures.
J Neurol Neurosurg Psychiatry. 2005 Jun 8; [Epub ahead of print]
The full text of this article is available for free from the link below:
Reuber M. Enright SM. Goulding PJ. Postoperative pseudostatus: not
everything that shakes is epilepsy. Anaesthesia. 55(1):74-8, 2000
Miller's Anesthesia. Ronald D. Miller Ed., 6th edition, Elsevier Publishing, 2005.