British Journal of Neurosurgery

ISSN: 0268-8697 (Print) 1360-046X (Online) Journal homepage: http://www.tandfonline.com/loi/ibjn20

A practical guide to the use of anti-epileptic drugs

by neurosurgeons

Fardad T. Afshari, Sophia Michael, Ismail Ughratdar & Shanika Samarasekera

To cite this article: Fardad T. Afshari, Sophia Michael, Ismail Ughratdar & Shanika Samarasekera
(2017) A practical guide to the use of anti-epileptic drugs by neurosurgeons, British Journal of
Neurosurgery, 31:5, 551-556, DOI: 10.1080/02688697.2017.1324618

To link to this article: https://doi.org/10.1080/02688697.2017.1324618

Published online: 08 May 2017.

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BRITISH JOURNAL OF NEUROSURGERY, 2017
VOL. 31, NO. 5, 551–556
https://doi.org/10.1080/02688697.2017.1324618

REVIEW ARTICLE

A practical guide to the use of anti-epileptic drugs by neurosurgeons

Fardad T. Afsharia, Sophia Michaelb, Ismail Ughratdara and Shanika Samarasekerab
a
Department of Neurosurgery, University Hospitals Birmingham, Birmingham, UK; bDepartment of Neurology, University Hospitals Birmingham,
Birmingham, UK

ABSTRACT ARTICLE HISTORY

Initiation of anti-epileptic drugs is increasingly relevant to daily neurosurgical practice. Intracranial patholo- Received 17 December 2016
gies ranging from brain tumours to subarachnoid haemorrhage and traumatic brain injury are commonly Revised 22 April 2017
associated with the subsequent development of seizures. The scope and range of anti-epileptic drugs Accepted 24 April 2017
available has increased dramatically in recent years and understanding the evidence base behind this class
of drugs in addition to their interaction/side effect profiles is essential. In this review we aim to generate a KEYWORDS
practical guide for neurosurgeons regarding the use of different anti-epileptic medications in common Epilepsy; seizure;
neurosurgical conditions, including considerations for their use in pregnancy. subarachnoid haemorrhage;
traumatic brain injury
Abbreviations: AED: Anti-epileptic drug; SAH: Subarachnoid haemorrhage; TBI: Traumatic brain injury

Anti-epileptic drugs, indications and side effects
Seizures are one of the major consequences of neuronal injury
and insult and can result from a diverse range of pathologies
including trauma, infection and malignancy. Seizures adversely
affect both the patient’s immediate recovery and longer term
quality of life.1 Use of anti-epileptic drugs (AEDs) is common
practice in neurosurgical centres. With the large number of AEDs
available, making the right choice of AED for each condition is
crucial and involves understanding their spectrum of use, side
effect and interaction profiles (Table 1). AEDs can be used as
prophylaxis or as treatment for seizures.
With over 25 AEDs now available, there is an increasing trend
towards preferential use of some drugs for specific seizure types
and seizure syndromes. Seizure onset is currently classified as
‘focal’ – originating within networks limited to one hemisphere
or ‘generalised’-originating at some point within, and rapidly
engaging, bilaterally distributed networks.1 Acquired structural
pathology will generally give rise to a focal epilepsy, ie seizures
which originate in one locus; they may subsequently rapidly gen-
eralise as the epileptiform network spreads bilaterally.
Historically, both focal and generalised seizures have been
treated with AEDs such as phenytoin, a sodium channel modula-
tor manufactured over 100 years ago which has the advantage of
a relatively rapid onset of action and availability as both oral and
intravenous formulations. Sodium Valproate came into use in the
1960s and has since being preferentially used for primary general-
ised epilepsies while carbamazepine (developed around the same
time) was the preferred choice for focal seizures. These older
AEDs, whilst their efficacy is well recognised, are associated with
significant systemic side effects and potential for drug interac-
tions. Phenytoin has a narrow therapeutic window with the
potential for circulating (non protein-bound) levels to rise to
potentially toxic levels, especially in those with established renal
or hepatic impairment. Phenobarbitone, Phenytoin and
Carbamazepine as ‘enzyme inducers’ and Sodium Valproate as an
‘enzyme inhibitor’ modulate activity of cytochrome P450 with
resulting impact on serum concentrations. Valproate encephalop-
athy is a recognised phenomenon arising from intoxication
secondary to high levels of this drug, for example in those with
pre-existing hepatic dysfunction.
Perhaps in response to these concerns, the past 30 years have
seen a raft of newer AEDs come into mainstream use, including
lamotrigine (developed in the 1990s) and levetiracetam, developed
a decade later. The choice between older versus newer generation
drugs depends on a range of factors as diverse as seizure type, indi-
vidual tolerability and local guidelines. The SANAD study compar-
ing older versus newer generation AEDs was seminal in
establishing comparative efficacy and tolerability profiles for some
of these agents.2 1721 patients with focal epilepsy were randomised
to receive carbamazepine, gabapentin, lamotrigine, oxcarbazepine
or topiramate. Results demonstrated that carbamazepine was
superior in efficacy to its alternatives, though the difference
between carbamazepine and lamotrigine did not reach statistical
significance. However, time to treatment failure was significantly
longer for lamotrigine, suggesting that it is better tolerated and
may therefore be the drug of choice in many patients.2 SANAD II
which began recruitment in 2013, compares the newer AEDs –leve-
tiracetam and zonisamide with lamotrigine and should provide fur-
ther evidence for refining the treatment of focal epilepsy.3
Prophylactic use of anti-epileptic drugs in neurosurgery
The evidence for prophylactic use of AED in neurosurgery is lim-
ited. Below, we aim to review the current evidence behind the
use of AEDs in different neurosurgical conditions.
Traumatic brain injury
Seizures can occur in up to 30% of traumatic brain injury
patients. Seizures in the acute phase post head trauma can lead to
an increase in intracranial pressure. Prolonged seizures can
increase metabolic demand and excitotoxicity, resulting in

CONTACT Fardad T. Afshari afsharifardad@googlemail.com Department of Neurosurgery, University Hospitals Birmingham, Birmingham, UK
ß 2017 The Neurosurgical Foundation
552 F. T. AFSHARI ET AL.

Table 1. Summary of common anti-epileptic drugs and side effect profiles.

Approximate Therapeutic
Name of drug Half life starting dose Average dose range () level () Significant side effects
Carbamazepine 20–55 hrs 200 mg 400-1600 mg in divided 6–12 mg/ml Leukopenia, diplopia, ataxia, Steven Johnson
Twice daily doses syndrome, SIADH, hepatitis, agranulocytosis,
nausea/ vomiting
Gabapentin 5–7 hrs 300 mg 900-3600 mg in divided Unknown Dizziness, somnolence, nystagmus, increased
Thrice daily. doses appetite
Lacosamide 12–13 hrs 50 mg 50-400 mg in divided Unknown Dizziness, vertigo, diplopia, rash, poor concen-
Twice daily doses tration, poor appetite
Lamotrigine 24 hrs 25 mg 25-400 mg Unknown Dizziness, somnolence, diplopia, rash, Steven
Once daily Johnson syndrome, increase in myoclonus
Levetiracetam 6–8 hrs 250 mg 1000–3000 mg in divided Unknown Lethargy, renal failure/ dysfunction, aggression
twice daily doses and low mood
Phenobarbital 5 days 1–3 mg/kg/day in 60–180 mg 15–30 mg/ml Sedation, cognitive impairment, respiratory
two divided doses depression , tolerance and dependence,
ataxia, megaloblastic anaemia
Phenytoin 24 hrs 300–400 mg 300–500 mg 10-20 mg/ml Hepatic dysfunction, megaloblastic anaemia,
Once daily cerebellar degeneration, Steven Johnson
syndrome, gingival hypertrophy, rash,
reduced cognitive function, osteomalacia
and rickets
Topiramate 15–25 hrs 25mg 25–400 mg Unknown Weight loss, dizziness, ataxia, renal stones,
Once daily poor concentration, oligohidrosis,
hyperthermia
Sodium Valproate 8–20 hrs 300 mg 600–2000 mg in divided 50–100 mg/ml Teratogenicity, somnolence, hair loss, tremor,
Twice daily doses weight gain, platelet dysfunction, pancrea-
titis, liver failure
Zonisamide 63-69 hrs 25 mg 50–500 mg 10–40 mg/ml Weight loss, renal calculi
Twice daily

secondary neuronal loss and reactive gliosis.2 Addressing seizure
control post head injury is a crucial aspect of improving longer
term outcome.
There is class I evidence to support the prophylactic use of
AEDs during the early phase following head injury (first 7 days);
use of prophylactic AEDs has no effect on late onset seizures.4
Although there are currently no specific studies investigating
prophylactic AEDs use in different types of head injury, prophy-
lactic AEDs are advocated for diffuse or focal traumatic brain
injury such as in the context of traumatic brain contusions or
acute subdural haematoma with injury to cortical tissue.
Conditions such as isolated extradural haematoma in the absence
of underlying brain injury do not necessarily warrant the use of
prophylactic AEDs and many neurosurgeons do not necessarily
initiate AEDs in this context. Currently, practice of prophylactic
AED use in traumatic brain injury among UK neurosurgical
centres is variable.
Recent prospective randomised studies have demonstrated that
levetiracetam and phenytoin are equally effective for the treat-
ment of seizures post head injury.4 Use of phenytoin was linked
to poorer neurological status as assessed by Glasgow Outcome
Scale and Disability Rating Score at 3 and 6 months post injury.5
In light of more favourable side effect profiles, AEDs such as lev-
etiracetam are now more widely used.
Brain tumours
20–40% of patients with a brain tumour initially present with
seizures, a further 40% may present with seizures during the
course of their illness.6,7 The likelihood of developing seizures in
the context of a brain tumour depends on a number of factors
including tumour location; seizures are more common in cortical
and temporal tumours. Certain histopathological tumour types
are more epileptogenic. Neurogliomas and gangliogliomas have a
seizure incidence of over 80%, oligodendrogliomas over 70%,
diffuse low-grade gliomas over 60%, and glioblastomas (GBMs)
over 40%.7
Prophylactic AEDs are commonly used for patients with brain
tumours; this includes their peri-operative use in those under-
going craniotomy.
A Cochrane review in 2008 identified five randomised con-
trolled trials which looked at the prophylactic use of AEDs such
as phenytoin, phenobarbital, and valproate in a total of 404 sub-
jects with brain tumours. There were no differences in seizure
outcome between prophylactic AEDs and placebo.8
A systematic review by Komotar 2011, concluded that
prophylactic use of AEDs during resection of supratentorial
meningiomas is of no benefit in preventing early or late phase
post-operative seizures.9 A Cochrane review in 2015 which
included 8 randomised controlled trials also concluded that there
is little evidence to suggest that AED treatment administered
prophylactically is effective in preventing post-craniotomy
seizures.10
Prophylactic use of AEDs in patients with brain tumours is
therefore of no clear benefit and should be avoided to minimize
drug-related side effects.
Subarachnoid haemorrhage
Up to a quarter of patients suffering subarachnoid haemorrhage
subsequently develop seizures.11 The majority of these seizures
occur at the time of ictus or during the early phase (within the
first two weeks).
There is insufficient evidence to support or refute the use of
antiepileptic drugs as seizure prophylaxis after subarachnoid
haemorrhage.12 Widespread use of prophylactic AEDs is not rec-
ommended. The American Stroke Association states that for
aneurysmal subarachnoid haemorrhage, prophylactic AEDs may
be considered during the post-haemorrhagic period (early phase)
and longer term if risk of seizures is deemed to be very high.12
Risk factors for seizure recurrence were identified as a history of
seizures, haematoma, parenchymal infarct and a middle cerebral
artery aneurysm.13

Brain abscess and empyema
Infective collections such as abscesses and empyemas are well rec-
ognised as potentially epileptogenic foci with seizures occurring
in up to a third of patients with brain abscess.14–16 In addition to
surgical evacuation of abscesses, specific attention to anti-micro-
bial regime and seizure control is therefore of paramount import-
ance. Quinolones such as ciprofloxacin may lower the seizure
threshold; potential interaction between enzyme inducing AEDs
and antibiotics also needs to be considered.
Recommendations regarding the use of AEDs in brain
abscesses and empyemas are based on level V evidence.15,16
Seizures can develop both in early and late phases following
development of an abscess with latencies as long as 5 years
reported.15 In light of this, some studies have recommended
prompt use of prophylactic AEDs to continue for at least
1 year.16 Discontinuation can be considered after that period if
no clinical evidence of seizures or no significant epileptogenic
activity can be demonstrated on electroencephalogram.16 There
are no guidelines with regards to which AEDs are more effective
in seizure control in brain abscesses and empyemas (Table 2).
Therapeutic use of anti-epileptic drugs in neurosurgery
In contrast to the relative lack of evidence regarding prophylactic
use of AEDs in neurosurgery, therapeutic use of AEDs for seizure
control is better established and constitutes an important part of
care of neurosurgical patients pre and post operatively. The
choice and duration of therapy are important considerations.
The available evidence is summarised below.
Traumatic brain injury
There are currently no level 1 studies comparing the efficacy of
different AEDs in post head injury epilepsy patients. Tolerability
and interaction profiles are two of the factors which need to be
considered when choosing an AED in this context. Phenytoin,
levetiracetam and valproate are some of the most commonly used
drugs in the management of seizures post head injury.
Brain tumours
Following a tumour related seizure, patients should be offered
AEDs. Although there is a lack of level 1 evidence to support the
choice of AEDs for the treatment of brain tumour related epi-
lepsy,17 there have been a number of studies over the past decade
considering the efficacy of a range of AEDs.
AEDs that are frequently selected as first-line therapy include
second-generation non-enzyme-inducing AEDs such as lamotri-
gine and levetiracetam.6 Sodium Valproate is frequently used as
adjunctive therapy. Use of levetiracetam in patients with seizures
Table 2. Summary of recommendations for the prophylactic use of AEDs.
Highest level Current recommendation for prophylactic
Condition of evidence AED use
Traumatic Level I Recommended for 1 week post head injury
Brain Injury
Brain Tumours Level I Not recommended
Subarachnoid Level III Long term use not recommended but may
Haemorrhage be considered in immediate post haem-
orrhagic phase if risk factors such as ICH
in temporal lobe
Brain Abscess/ Level V Recommended
Empyema
BRITISH JOURNAL OF NEUROSURGERY 553
secondary to brain tumours has been shown to lead to greater
than 50% reduction in seizure frequency in 65% to 90% of
patients.6,17–19 Levetiracetam and sodium valproate have both
been suggested as monotherapies with good seizure control
profile
In patients with glioblastoma, sodium valproate has been sug-
gested to be associated with an improvement in survival of up to
three months as reported in The European Organization for
Research and Treatment of Cancer (EORTC) study.20 Its impact
at a cellular level on histone deacetylase inhibition has been
postulated to be responsible for its effect on tumour suppressor
genes activity.7 Both Levetiracetam and Sodium Valproate may
interact with Temozolamide (TMZ) chemotherapy, Sodium
Valproate as an enzyme inhibitor increases TMZ levels, which
may have a potential favourable effect on tumour regulation.
Blood monitoring should be undertaken in patients receiving
both sodium valproate and chemotherapy as potential interaction
can cause blood dyscrasias including thrombocytopaenia.
A particularly difficult decision post tumour resection is the
timing of withdrawal of AEDs in seizure free patients. Data about
the longer term consequence of AEDs withdrawal is limited and
therefore AED withdrawal in brain tumour patients is generally
not recommended without specialist neurology team input. In
addition data from studies on AEDs withdrawal for generalised
seizures may not be applicable or relevant to seizures caused by
brain tumours. In a retrospective study by Das et al, it was dem-
onstrated that 9.9% of patients post withdrawal of AEDs had
seizures post- excision of primary brain tumours and meningio-
mas over a median follow up period of 3.1 years.21 There were
no significant differences in seizure frequency post withdrawal of
AED between primary brain tumours and meningiomas. AED
continuation was strongly correlated with known risk factors for
developing postoperative seizures, namely preoperative seizures,
recurrence, incomplete resection, and temporal location.21
Further studies are needed to stratify the risk of seizures among
those perceived as potentially lower risk of ongoing symptoms.
Subarachnoid haemorrhage
Currently there is lack of level 1 evidence regarding the use of
AEDs in preventing epilepsy secondary to subarachnoid haemor-
rhage.12 Seizures post subarachnoid haemorrhage are commonly
treated and AED use in this context is recommended. A min-
imum of two years seizure freedom is generally considered neces-
sary prior to considering AED withdrawal.
Brain abscess and empyema
AEDs are clearly indicated for the treatment of seizures compli-
cating cerebral abscesses and empyemas (Level V evidence).15,16
In keeping with seizures post subarachnoid haemorrhage, at least
two years of seizure freedom is generally considered necessary
before AEDs can be tapered to withdrawal (Table 3).16
Table 3. Summary of recommendations for the therapeutic use of AEDs.
Level of Evidence for Current recommendation
Condition therapeutic AED use for therapeutic AED use
Traumatic Level V Recommended
Brain Injury
Brain Tumours Level V Recommended
Subarachnoid Haemorrhage Level V Recommended
Brain Abscess/ Empyema Level V Recommended
554 F. T. AFSHARI ET AL.
Surgical perspectives regarding the management of
status epilepticus
Status epilepticus (SE) is a medical emergency and is a common
occurrence in the critically ill neurosurgical patient. Status epilep-
ticus is defined as 5 min or more of continuous clinical or elec-
trographic seizure activity or recurrent seizure activity without
recovery between seizures.22 This is based on evidence that clin-
ical and electrographic seizures lasting longer than 5 mins often
do not stop spontaneously.22 The treatment of status epilepticus
by convention occurs in 3 stages. These include emergent initial
therapy, urgent control therapy and refractory therapy. Definitive
control of status epilepticus should be established within
60 minutes of onset.
Following initial assessment and management of airway,
breathing and circulation, emergent treatment should be initiated.
This involves intravenous benzodiazepines. For intravenous ther-
apy, lorazepam is the preferred agent. Other options include
midazolam for intramuscular therapy and diazepam for rectal
administration.22,23 The Rapid Anticonvulsant Medication Prior
to Arrival Trial (RAMPART) study comparing the use of intra-
muscular midazolam versus intravenous lorazepam as the active
control in pre-hospital SE, showed that midazolam was at least as
efficacious as lorazepam.24
Urgent control therapy serves two aims, rapid achievement of
therapeutic anti-epileptic levels in patients who have responded
to emergent treatment and seizure control in those who have
failed to respond. Most commonly used agents for this stage of
treatment include, phenytoin, sodium valproate, levetiracetam.22
In patients who are already on AEDs, an intravenous bolus of
their usual AED is advisable before addition of another agent.
This is to ensure therapeutic levels.22
Treatment of refractory status epilepticus (RSE)- that which
persists in spite of benzodiazepines and anticonvulsant therapy,
involves escalation with involvement of critical care and admis-
sion to the intensive care unit. This enables initiation of anaes-
thetic agents including propofol, phenobarbital and in some
countries use of thiopental.22 There is insufficient data to suggest
superiority of one of these agents.25
Data is emerging regarding the role of intracranial stimulation
in the management of super refractory status epilepticus (SRSE),
defined as status which persists or recurs in spite of 24 hours or
more of anaesthetic therapy.26 Deep brain stimulation of centro-
median thalamic nuclei has been reported to be a potential target
for controlling drug refractory seizures.27
Considerations regarding the use of AEDs in pregnancy
Teratogenicity
AEDs have been linked to anatomical anomalies and teratogen-
esis.28 The most common AED-related malformations are cardiac,
followed by orofacial clefts, neural tube defects (spina bifida and
anencephaly), skeletal, and urogenital defects; valproate in par-
ticular has been associated with spina bifida. Postulated terato-
genic mechanisms include reduced enzyme activity, direct AED
neuronal toxicity, and AED-induced folate deficiency.28,29
The incidence of major congenital malformations in infants
born to mothers taking AEDs is around 4–6%, compared to
2–4% in the general population.28,29 Studies of AEDs in preg-
nancy are limited with heterogeneity of data, and inadequately
powered, thus comparative risks of malformations for individual
drugs remain largely undefined. Lamotrigine is the most studied
agent of the new AEDs in pregnancy, with international
databases of class 2 evidence reporting a 2.9% rate of birth
defects in monotherapy exposures. This rate appears to be similar
with levetiracetam monotherapy. Despite their safer profile, there
remains uncertainty regarding effect of higher doses of such
drugs in pregnancy. In contrast, valproate use increases risk of
congenital malformations (10.7%). Sodium valproate teratogen-
icity is dose-dependent, with significant risk in maternal daily
dosage 1000mg; the UK and EURAP International Epilepsy and
Pregnancy Registry data suggest that dose-dependent teratogen-
icity is true for some AEDs.30,31 Polytherapy, particularly regi-
mens including sodium valproate, poses increased risk of fetal
malformations and cognitive deficits (up to 15% with two or
more AEDs).32 Risk of cognitive deficits appears to be highest in
sodium valproate exposure, and lowest with lamotrigine, levetira-
cetam and carbamazepine.28–30,33
Seizure control
Seizure control is crucial during pregnancy and should be man-
aged in joint consultation with a neurologist and obstetrician.
Maternal physiological changes in pregnancy (increased blood
volume, increased glomerular filtration rate, and lower albumin
concentrations and therefore drug binding) can modify the
pharmacokinetics of AEDs. Serum AED concentrations may fall
resulting in breakthrough seizures, which pose risks to both the
mother and foetus (foetal bradycardia, hypoxia and death).
Maternal factors, such as pregnancy- related emesis, may influ-
ence bioavailability. During pregnancy, AED plasma concentra-
tion monitoring should be considered, especially if seizures
become uncontrolled. Examples are lamotrigine and levetirace-
tam; dose escalation may be substantial in order to maintain opti-
mum therapy.29 Post-partum, levels can rapidly rise with the
potential for toxicity and prompt dose adjustments may be
required under the guidance of a neurologist.
Pregnancy may stimulate growth of tumours possessing
steroid hormone receptors such as meningiomas, or trigger
worsening peri-tumoural oedema leading to seizures and some-
times first presentation of a brain tumour.
Folic acid
Folate deficiency is associated with neural tube defects and there-
fore supplementation of diet with folic acid is advised before con-
ception. Folate supplementation is particularly important in
epileptic women during pregnancy as AEDs may further increase
the risk of faetal neural tube defects. High-dose folic acid (5 mg
daily) should be taken during pre-conception until at least the
end of the first trimester.32
Lifestyle guidance for patients with epilepsy
It is essential that patients with seizures are fully informed regard-
ing the treatability of seizures and the importance of adherence to
AED therapy. Patients should be counselled regarding the side
effects of AEDs and the need to tailor the AED to the patient’s
individual tolerability profile. This process may take time.
Patients with epilepsy should be encouraged to continue to
lead a full and active life; nevertheless the risks around certain
activities including bathing, working with machinery or at heights
should be explored. Patients need to be aware of the relatively
rare (less than 1 in 1000) incidence of sudden death in epilepsy
(SUDEP), more commonly associated with generalised seizures,

especially those occurring during sleep.34 Compliance with AEDs,
night-time supervision and education of carers can help to reduce
the risk of SUDEP.35
Those in employment are encouraged to discuss their condi-
tion with their employers in order to optimise their working
environment and allow safe working conditions. This includes
optimising shift patterns to ensure that good sleep hygiene is
maintained. Patients are obliged to notify the Driver and
Vehicle Licensing Agency (DVLA) following a single seizure
and/or neurosurgical procedure. Driving restrictions can impact
substantially on a patient’s livelihood; charities such as Epilepsy
Action and the Epilepsy Society can provide support in this
regard.
Summary points
Use of AEDs as prophylaxis reduces the risk of early seizures
(within the first 7 days) post head injury with no effect on late
onset seizures (Level 1).
Use of AEDs for treatment of seizures post head injury is clin-
ically indicated (Level 5).
Prophylactic use of AEDs in brain tumours are not recom-
mended (Level 1).
In spite of the paucity of evidence regarding the therapeutic
use of AEDs for seizures complicating intracerebral neoplasm,
subarachnoid haemorrhage and cerebral abscess, AEDs are rec-
ommended for these conditions and are generally commenced
following a single seizure (Level 5).
Treatment strategies for status epileptics should constitute
emergent initial therapy, urgent control therapy and refractory
therapy. Once the seizure control has been achieved, the underly-
ing cause needs to be urgently investigated and rectified.
Regarding the choice of AEDs in pregnant women with epi-
lepsy, cumulative data suggests that sodium valproate confers a
higher risk of teratogenesis compared with alternative agents
including lamotrigine and levetiracetam. Polytherapy regimes,
particularly those including sodium valproate, are associated with
higher risk of teratogenesis compared to monotherapy; it should
be borne in mind that risk of teratogenicity is generally dose-
dependent. Pregnant patients with intracranial pathology should
be promptly referred into a joint neurology/obstetric clinic, both
to ensure close monitoring during pregnancy and to facilitate
planning around delivery.
The majority of patients with focal epilepsy can attain reason-
able seizure control with antiepileptic therapy. Seizures are a
major cause of morbidity and their treatment can dramatically
improve quality of life.
Disclosure statement
Authors report no conflict of interest.
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