CLINICAL ASSESSMENT IN NEUROLOGY
Epilepsy: diagnosis,
classification and
management
Lauren Harris
Heather Angus-Leppan
Abstract
Careful clinical evaluation differentiates epileptic seizures from syn-
cope (vasovagal and cardiogenic), dissociative seizures (non-epileptic
attack disorder) and other rarer causes of paroxysmal events. The
initial diagnosis of epilepsy is incorrect in 20e30% of patients. Inves-
tigations can include blood tests, electrocardiograms, electroenceph-
alograms and neuro-imaging. Patients should be informed and
counselled about the diagnosis. Anti-epileptic drugs are the first-line
treatment for epilepsy, the choice depending on the epilepsy syn-
drome, the seizure type, the patient and their co-morbidities. Surgical
options are available for refractory epilepsy. Status epilepticus is a
medical emergency and all clinicians should be aware of the treatment
algorithm.
Keywords Anti-epileptic drug; epilepsy; focal; generalized; MRCP;
seizure; status epilepticus
Introduction
A seizure is a clinical manifestation of ‘abnormal excessive or
synchronous neuronal activity in the brain’. Manifestations range
from a brief sensation of ‘deja vu’ to a toniceclonic seizure, and
can involve altered sensation, perception, motor function,
behaviour or consciousness.1 The new International League
Against Epilepsy (ILAE) definition adds points (2) and (3) to the
previous definition:
(1) two or more unprovoked (or reflex) seizures occurring >24
hours apart
(2) one seizure and >60% chance of another seizure over the
next 10 years (judged by clinical features and investigations)
(3) diagnosis of an epilepsy syndrome (based on clinical features
and investigations).
Epilepsy is considered to have resolved after 10 seizure-free
years with no anti-epileptic drug (AED) taken for the previous
Lauren Harris MBBS MRCS is a Neurosurgical Trainee in the North
Thames of London, UK. Competing interests: none declared.
Heather Angus-Leppan MBBS (Hons) MSc MD FRACP FRCP is a
Consultant Neurologist and Epilepsy Initiative Group Lead at the
Royal Free London NHS Trust, and Honorary Consultant at UCL
Institute of Neurology, London, UK. Competing interests: Her salary
is part paid by the National Institute for Health. Non-pharmacological
research support from Eisai, Epilepsy Action and Royal Free Charity,
and Honoraria from Eisai, Combigene and UCB outside this work.
She has been on advisory boards for MHRA, Association of British
Neurologists, Royal College of Physicians and Sanofi women and
epilepsy education boards.
MEDICINE 48:8
Key points
C It is important to differentiate epilepsy from ‘mimics’, espe-
cially syncope and dissociative seizures, and clinical assess-
ment is essential
C Investigation for seizures includes blood tests, electrocardio-
grams, electroencephalograms and neuro-imaging. Genetic
testing will be increasingly used for precision diagnosis
C Anti-epileptic drugs are the first-line choice in treatment,
tailored to the patient, their co-morbidities, the epilepsy syn-
drome and the seizure type. Surgical options are available for
refractory focal epilepsy
C Status epilepticus is a medical emergency
5 years. About 0.5e1% of the population have active epilepsy,
5% have febrile seizures, and the lifetime prevalence of other
seizures is 2e5%.2
Differential diagnosis
The correct diagnosis is vital (Table 1). Missing epilepsy can
result in further untreated, potentially fatal, seizures. An erro-
neous diagnosis exposes a person to treatment with AEDs (with
associated adverse effects) and social costs (e.g. driving ban,
swimming restrictions).
Vasovagal (reflex) syncope is the most common cause of
transient loss of consciousness (‘blackouts’), often with a trigger
(including postural hypotension). Cardiogenic syncope is serious
(chiefly arrhythmias, myocardial or valvular heart disease) and
usually occurs without warning.
About 10% of ‘blackouts’ are dissociative seizures (also called
functional seizures, non-epileptic attack disorder, psychogenic
seizures and, previously, ‘pseudo-seizures’). More common in
female patients, they can coexist with epilepsy. There is inter-
action during episodes, such as resistance to eye opening, with
rapid recovery. Previous physical, emotional or sexual abuse is
frequent. Correct diagnosis takes an average of 7 years in the UK,
and patients can be wrongly classed as having refractory epilepsy
after multiple trials of AEDs.
Other differential diagnoses for toniceclonic seizures include
delirium, metabolic disturbance and breath-holding attacks in
young children. Focal seizures can be confused with migraine
aura, transient ischaemic attack, transient global amnesia,
paroxysmal movement disorder, tics, or tonic spasms of multiple
sclerosis. Nocturnal seizures can mimic parasomnias (hypnic
jerks, rapid eye movement sleep behaviour disorder, sleep-
walking, narcolepsy, night terrors, periodic limb movements).3
Classification
The 2017 ILAE classification of epilepsy is a three-level classifi-
cation system, reflecting that epilepsy is not simply a symptom of
local brain abnormality, but a network disease. Seizures can
arise from neocortical, thalamocortical, limbic and brainstem
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 CLINICAL ASSESSMENT IN NEUROLOGY

Differentiating epileptic seizures from non-epileptic attack disorder, vasovagal syncope and cardiogenic syncope
Epileptic seizures Non-epileptic attack disorder Vasovagal syncope Cardiogenic syncope

Trigger Alcohol, sleep deprivation Common e stress/emotion Common e stress, Rare

related standing,
heat, excitement
During sleep Common Never from established Never Unknown
sleep, but can occur in bed Can present as
sudden death
Onset Sudden Gradual (minutes) Gradual (minutes) Sudden
Aura/prodrome Various, stereotyped Change in mental state, Nausea, blurred vision, Uncommon
fear, panic epigastric sensation, heat,
headache, tinnitus,
palpitations, sweating
Speech Cry, grunt Variable, often Nil Nil
Words in automatisms unintelligible
Movements Stereotyped Asynchronous, flailing, Flaccid Usually flaccid
Atonic, tonic, clonic thrusting, opisthotonus, Can have myoclonic jerks, Can have myoclonic
(synchronous, small change in amplitude, rarely tonic or clonic jerks, tonic or clonic
amplitude, high side-to-side head movements movements
frequency) movements
Eyes Open Closed, active resistance Closed or rolled back Closed or rolled back
to eye opening
Injury Tongue biting (lateral), Directed violence and Fall Fall
fall, can have serious injury not uncommon, Tongue biting rare Tongue biting rare
injuries e.g. burns/fractures may bite tongue (tip,
not laterally)
Awareness Depends on seizure type Retained reactivity and Loss Loss
Loss in tonic clonic not unconscious
Response to Depends on seizure type, Reacts, this can terminate None None
stimulation none in toniceclonic the attack
Complexion Cyanosis Unchanged Pale Pale
Incontinence Common Occasional Occasional Occasional
Duration Minutes Minutes to prolonged Seconds (<1 minute) Variable
Evolution of seizure Continuous Fluctuating e e
Blood results Raised white cell count, Normal Normal Normal
prolactin and lactate
concentrations
Recovery Confusion >10 minutes if Variable, can be rapid Rapid recovery, pale, cold, Rapid recovery unless
generalized tonic clammy, fatigue sudden death
eclonic seizure Pale, cold, clammy

Table 1

networks. It replaces a simpler classification, and many patients hallucinations, illusions, perceptual distortions). Hyperkinetic
and clinicians remain unfamiliar with it (Table 2). activity is agitated thrashing or leg-pedalling movements.

Level 1 e seizure type Level 2 e epilepsy type

This can be classified into focal, generalized or unknown onset.
Focal seizures originate from within one hemisphere, whereas
generalized seizures involve both from the outset.
Seizure types are further classified (Table 3). For example, a
seizure that starts with an emotional response but progresses to
focal tonic activity is a focal emotional seizure (progressing to
tonic). Cognitive (dyscognitive) seizures can be ‘negative’ (loss
of function such as aphasia) or ‘positive’ phenomena (deja vu,
The diagnosis is clinical, supported by electroencephalography
(EEG). In generalized epilepsy, the patient typically has gener-
alized spikeewave activity on EEG. In focal epilepsy, epilepti-
form discharges are unilateral and localized, although the EEG is
often normal between seizures. Combined generalized and focal
epilepsy, a new group, recognizes that some patients have both
epilepsy types, as in Dravet or LennoxeGastaut syndrome.

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 CLINICAL ASSESSMENT IN NEUROLOGY

The change in terminology for seizure type

New term Old term

Focal aware seizure Aura (simple partial seizure)

Focal impaired awareness seizure Complex partial seizure
Focal dyscognitive seizure A type of complex partial seizure involving abnormal cognitive functioning
Focal to bilateral toniceclonic Partial (focal) onset with secondary generalization

Table 2

Level 3 e epilepsy syndrome
This refers to a cluster of features, incorporating seizure type,
EEG and imaging findings. It is often age dependent and can have
distinct co-morbidities including intellectual disability, psycho-
logical and behavioural problems.
Idiopathic generalized epilepsies (also known as genetic
generalized epilepsies) include:
 childhood absence epilepsy
 juvenile absence epilepsy
 juvenile myoclonic epilepsy
 generalized toniceclonic seizures alone.
Self-limiting focal epilepsies include:
 self-limited epilepsy with centrotemporal spikes
 occipital epilepsies of childhood (Panayiotopoulos and
LennoxeGastaut syndromes).
The term ‘self-limiting’ has replaced the old term ‘benign’.
Aetiology
Epilepsy can have more than one aetiology.
Structural e acquired causes include cerebrovascular dis-
ease, trauma, infection, space-occupying lesions (benign,
metastasis, glioma). Mesial temporal lobe seizures with hippo-
campal sclerosis may be amenable to surgery. Malformations of
cortical development (sometimes genetic) are increasingly
recognized with magnetic resonance imaging (MRI) scanning.
Genetic e genetic epilepsy results from a known or presumed
genetic mutation in which seizures are a core symptom of the
disorder, either inherited or de novo. Genetic generalized epi-
lepsy (idiopathic epilepsy), the most common, makes up 25% of
epilepsies. A structural aetiology can have a genetic basis, such
as tuberous sclerosis complex, and both aetiological terms can be
used.
Infectious e this is the most common aetiology worldwide
and includes meningitis and encephalitis. Infections include
malaria, neurocysticercosis, tuberculosis, HIV, toxoplasmosis
and cytomegalovirus.
Metabolic e these include hypoxiceischaemic encephalopa-
thy, porphyria, uraemia, aminoacidopathies and pyridoxine-
dependent seizures.
Immune e early recognition and treatment with immuno-
suppression are essential for these conditions, which include
anti-N-methyl-D-aspartate (NMDA) receptor and anti-leucine-rich
glioma-inactivated 1 (LGI1) encephalitis.
Unknown e this was previously referred to as cryptogenic.
Investigation
A full history, from both the patient and witnesses, includes
prodromal symptoms, triggers, time and environment of the
seizure, duration, progression, ictal and post-ictal events and
drug, alcohol and family history.

ILAE 2017 classification of seizure type

Focal onset Generalized onset Unknown onset
Aware/impaired awareness Motor onset Motor onset
Motor onset C Toniceclonic C Toniceclonic
C Automatisms C Clonic C Epileptic spasms
C Atonic C Tonic Non-motor
C Clonic C Myoclonic C Behaviour arrest
C Epileptic spasms C Myoclonicetoniceclonic
C Hyperkinetic C Myocloniceatonic
C Myoclonic C Atonic Unclassified
C Tonic C Epileptic spasm
Non-motor onset Non-motor onset (absence)
C Autonomic C Typical
C Behaviour arrest C Atypical
C Cognitive C Myoclonic
C Emotional C Eyelid myoclonia
C Sensory
Focal to bilateral toniceclonic

Table 3

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 CLINICAL ASSESSMENT IN NEUROLOGY

Neurological and cardiovascular examination should include
lying and standing blood pressure if syncope is suspected.
Recorded evidence of the episode (from videos or, with the pa-
tient’s permission, on an eyewitness’s phone) can be diagnostic.
An electrocardiogram (ECG) is mandatory, looking for
arrhythmia, ischaemic changes or heart block.
Electrolyte abnormalities including hyponatraemia, hypo-
glycaemia, hypocalcaemia and thyroid disease can cause or
trigger a seizure. Elevated white cell count and lactate and pro-
lactin concentrations often occur with seizures but are not
diagnostic. Anaemia predisposes to syncope. Liver and renal
function should be checked, particularly before AED treatment.
Further tests are tailored to the clinical situation. If cardiac
syncope is suspected, a cardiologist review and 24-hour tape or
transthoracic echocardiogram should be urgently arranged. In a
pregnant woman, eclampsia must be considered. Antineuronal
antibodies and gene mutations may be investigated by the epi-
lepsy specialist if indicated.
A normal EEG is seen in 50% of people with epilepsy and
should not be used in isolation.3 It helps to determine the seizure
type (focal versus generalized), to assess the risk of seizure
recurrence and the response to treatment. In genetic (idiopathic)
generalized epilepsy, a 3-s spike and wave pattern is present in
98% of patients. EEG is useful in intensive care settings to assess
seizure activity in intubated, paralysed patients. Sleep-deprived
EEGs and video or ambulatory EEGs (video-telemetry) can be
used if a standard EEG (including photic stimulation and hy-
perventilation) is inconclusive or surgery is being considered.
MRI is the imaging of choice, with specific epilepsy protocols
to identify subtle structural lesions. Computed tomography scans
investigate acute neurological injury (trauma, haemorrhage,
unconscious patient). MRI is not required for a diagnosis of ge-
netic (idiopathic) generalized epilepsy if the clinical features and
EEG results are typical.
Potential surgical candidates require precise functional iden-
tification of the seizure focus, with video-telemetry and high-
resolution MRI. Positron emission tomography to identify
hypometabolism, single-photon emission tomography to identify
increased blood flow, and magnetoencephalography for func-
tional imaging can be used. Neuropsychological testing with
functional imaging (MRI) can lateralize the dominant hemi-
sphere and assess memory. In selected cases, invasive EEG
identifies the focus via depth electrodes placed stereotactically or
with subdural grids.
Management
Patients should be assessed by specialists, with a comprehensive
care plan and ideally including access to an epilepsy specialist
nurse.

AED option by seizure type as directed by National Institute for Health and Care Excellence guidelines
Seizure type First-line AEDs Adjunctive AEDs Other options for tertiary care

Generalized toniceclonic Sodium valproate Clobazam

Lamotrigine Lamotrigine
Carbamazepine Levetiracetam
Oxcarbazepine Sodium valproate
Topiramate

Tonic or atonic Sodium valproate Lamotrigine Rufinamide

Topiramate

Absence Ethosuximide Ethosuximide Clobazam

Lamotrigine Lamotrigine Clonazepam
Sodium valproate Sodium valproate Levetiracetam
Topiramate
Zonisamide

Myoclonic Sodium valproate Levetiracetam Clobazam

Levetiracetam Sodium valproate Clonazepam
Topiramate Topiramate Piracetam
Zonisamide

Focal Carbamazepine Carbamazepine Eslicarbazepine acetate

Lamotrigine Clobazam Lacosamide
Levetiracetam Gabapentin Phenobarbital
Oxcarbazepine Lamotrigine Phenytoin
Sodium valproate Levetiracetam Pregabalin
Oxcarbazepine Tiagabine
Sodium valproate Vigabatrin
Topiramate Zonisamide

Table 4

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 CLINICAL ASSESSMENT IN NEUROLOGY

Emergency treatment of status epilepticus for adults

Step Time

1 0 min ABC Confirm epileptic seizure clinically

2 <5 min
3 5e15 min
4 >30 min
Turn patient onto their side
High-flow oxygen
Check blood glucose
Check cardiorespiratory function
Establish i.v. access
Midazolam 0. 5 mg/kg (usually 10 mg) ebuccal Midazolam available out of hospital
Or lorazepam 0.1 mg/kg (4 mg) e i.v. Call for senior help
Or diazepam 0.2e0.5 mg/kg (10e20 mg) e rectal
Repeat loading dose if necessary after 10 minutes (maximum one repeat)
Give 50% glucose 50 ml or thiamine 100 mg i.v. (or Pabrinex) if required
Phenytoin 15e20 mg/kg i.v. over 20 minutes ICU in attendance
Or fosphenytoin 15e20 mg/kg i.v.
Or Phenobarbital 20 mg/kg i.v. over 5 minutes
Or levetiracetam 20e60 mg/kg i.v. over 15 minutes
Or sodium valproate 20e40 mg/kg i.v.
Rapid sequence induction of anaesthesia thiopental sodium 4 mg/kg i.v. Transfer to ICU
Or propofol 2 mg/kg i.v. loading dose then 2e5 mg/kg/hour Assess underlying cause
Or midazolam 0.2 mg/kg i.v. loading dose then 0.2e0.6 mg/kg/hour

Treat in a stepwise manner. Times vary depending on guideline used.

ABC, Airway, Breathing, Circulation management as per adult life support; ICU, intensive care unit; i.v., intravenous.

Table 5

Patients need information about:
 the nature of epilepsy, and sources of information
 avoiding triggers (e.g. alcohol, sleep deprivation)
 risk and prevention of injury and sudden unexplained
death in epilepsy.4
 swimming or bathing unsupervised (avoiding having a
bath alone)
 driving e UK patients must contact the Driver and Vehicle
Licensing Agency (usually a 1-year ban, depending on
seizure type)
 working at heights or climbing
 cooking over an unguarded oven or fire
 using heavy machinery
 using trains e stand at the back of the platform
 child care e feeding, carrying, bathing (to avoid bathing a
baby alone).
Anti-epileptic drug therapy
AED therapy with tolerable adverse effects can achieve seizure
control in 60e75% of people with epilepsy.
AED treatment should be individualized according to the
seizure type, epilepsy syndrome, co-morbidities and patient,
aiming for monotherapy (Table 4). Carbamazepine, oxcarbaze-
pine and lamotrigine can worsen myoclonic and absence sei-
zures. The selected medication is titrated until the seizures are
controlled or adverse effects occur. If treatment is unsuccessful, a
second drug is titrated to an adequate dose, and the first drug
then usually tapered off slowly. Combination therapy is some-
times needed.
Informed patient choice requires information on the risks and
benefits of different AEDs (and of not having treatment). Women
of child-bearing age need information about contraception
(including the interaction of hepatic enzyme-inducing AEDs with
the oral contraceptive pill) and pregnancy (because of the need to
balance personal safety with the increased incidence of fetal
malformations). Sodium valproate has additional safety advice
because of the risk of neurodevelopmental impairments in the
fetus; it is therefore often used as a drug of last resort. However,
it is the most effective medication for idiopathic generalized ep-
ilepsy, and stopping valproate can significantly worsen seizure
control.5
Monitoring of AED blood levels is recommended to detect
non-adherence or toxicity, to adjust the phenytoin dose and to
manage pharmacokinetic interactions. A full blood count, elec-
trolytes, liver enzymes, vitamin D concentrations and bone
profile should be measured every 2e5 years if the individual is
on enzyme-inducing drugs. Valproate can interfere with clotting,
and this should be checked preoperatively.
Withdrawing AEDs needs specialist input. There is no
consensus, but in general it can be considered after at least 2
years free of seizures. A higher risk of relapse is associated with
the severity of the seizure disorder, neurological deficits,
abnormal EEG and/or imaging, intellectual disability, age of the
patient and previous failed attempts. It should be done over at
least 2e3 months, withdrawing one drug at a time. If a seizure
occurs, the last dose reduction is reversed. Withdraw the most
sedating drug first. Most recurrence occurs in the first 3e6
months after withdrawal.

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 CLINICAL ASSESSMENT IN NEUROLOGY
Newer potential treatment targets for epilepsy are being
developed, for example mammalian target of rapamycin (mTOR)
inhibitors in patients with tuberous sclerosis.
A ketogenic diet can benefit both children and adults. Psy-
chological interventions (relaxation, cognitive behavioural ther-
apy) can be used alongside medication.
Surgical treatment
Surgical options are considered for medically refractory seizures
despite appropriate treatment with AEDs for at least 1 year
(usually failed two attempts with high-dose monotherapy and
one polytherapy).
Three categories of patients are suitable, those with:
 focal seizures e mesial temporal lobe epilepsy (MTLE) or
extratemporal epilepsy
 symptomatic generalized seizures, such as Lennox
eGastaut syndrome
 unilateral, multifocal epilepsy associated with infantile
hemiplegia syndrome.
There are three types of procedure:
 Resection e the most common resection is anterior tem-
poral lobectomy or amygdalo-hippocampectomy for MTLE
or the specific lesion (hippocampal sclerosis, tumour,
cavernoma), with up to 80% success in completely con-
trolling seizures.
 Disconnection e this is used if eloquent brain is involved
or to separate the activity of the two cerebral hemispheres.
This includes a corpus callosotomy (for generalized major
motor seizures), hemispherectomy (for focal seizures with
widespread hemispheric lesions) and multiple subpial
transection (for focal seizures in eloquent cortex).
 Stimulation e this is an adjunctive therapy for patients
not suitable for resective surgery. It is reversible and
adjustable, and offers 30e40% seizure reduction. It in-
cludes vagus nerve stimulation, deep brain stimulation and
closed-loop stimulation.
The treatment of status epilepticus
Status epilepticus is a continuous seizure lasting >5e30 min
(definitions vary) or persistent seizure activity after sequential
administration of appropriate first- and second-line AEDs. Any
seizure type can progress to status epilepticus. The most com-
mon cause is missed medication in a patient with epilepsy.
Symptomatic causes such as infection, febrile seizures, alcohol
TEST YOURSELF
To test your knowledge based on the article you have just read, please complete the questions below. The answers can be found at the
end of the issue or online here.
Question 1
A 17-year-old girl presented after three episodes of ‘blackouts.’ In
each episode, she had been standing, had initially felt dizzy and
MEDICINE 48:8
withdrawal, trauma, strokes, metabolic disturbance and hypoxia
are other aetiologies.
Toniceclonic (convulsive) status epilepticus has a high
morbidity and mortality related to cause and duration. After 20
minutes of repetitive electrical discharge, irreversible changes
occur in central nervous system neurones. Cell death and sys-
temic stress response is common after 1 hour.
Acute toniceclonic seizures are a medical emergency. Treat-
ment should stabilize the patient, stop the seizure and identify
the cause following the algorithm shown in Table 5. A
KEY REFERENCES
1 Angus-Leppan H. First seizures in adults. Br Med J 2014; 348.
https://doi.org/10.1136/bmj.g2470.
2 Angus-Leppan H, Parsons LM. Epilepsy: epidemiology, classifi-
cation and natural history. Medicine (Baltim) 2008; 36: 571e8.
3 Angus-Leppan H. Migraine: mimics, borderlands and chameleons.
Practical Neurol 2013; 13: 308e18.
4 Keddie S, Angus-Leppan H, Parker T, et al. Discussing sudden
unexpected death in epilepsy: are we empowering our patients? A
questionnaire survey. JRSM Open 2016; 7: 205427041665435.
5 Marson AG, Burnside G, Appleton R, et al. The SANAD II study of
effectiveness of valproate or levetiracetam in generalised and un-
classifiable epilepsy: an un-blinded randomised controlled trial. In:
International epilepsy congress, June 22e26 2019. Bangkok,
Thailand. Abstract 1027.
FURTHER READING
Fisher RS, Acevedo C, Arzimanoglou A, et al. ILAE Official Report: a
practical clinical definition of epilepsy. Epilepsia 2014; 55: 475e82.
Fisher RS, Cross JH, French JA, et al. Operational classification of
seizure types by the International League Against Epilepsy: position
paper of the ILAE commission for classification and terminology.
Epilepsia 2017; 58: 522e30.
Harris L, Lowes O, Angus-Leppan H. Treatment decisions in women of
childbearing age on valproate. Acta Neurol Scand 2020; 141:
287e93. https://doi.org/10.1111/ane.13211.
Kapur J, Elm J, Chamberlain JM, et al. Randomized trial of three
anticonvulsant medications for status epilepticus. N Engl J Med
2019; 381: 2103e13.
National Institute for Health and Care Excellence. Epilepsies: diagnosis
and management. CG137, https://www.nice.org.uk/guidance/
cg137 (accessed 28 March 2020).
her vision had dimmed. She had then fallen to the ground, pale,
and some had witnessed ‘shaking’ in her arms and legs. She had
lost consciousness for 30 seconds, and had been incontinent of
527 Ó 2020 Published by Elsevier Ltd.
 CLINICAL ASSESSMENT IN NEUROLOGY
urine. After the episode, she had sat up immediately and had
been alert and orientated but complaining of headaches. She was
otherwise well but her mother had died 3 months previously.
Clinical examination was normal.
What is the most appropriate management at this stage?
A. Arrange an ECG, electroencephalography (EEG) and MRI of
the brain, discuss safety measures and commence anti-epi-
leptic drugs as she has had three episodes
B. Arrange an ECG and reassure her that her symptoms are
benign
C. Diagnose dissociative attacks and refer her to a psychiatrist
D. Arrange investigations and follow-up soon as the diagnosis
is unclear
E. Reassure her that her symptoms are likely to be caused by
life stress and offer guidance and counselling as
appropriate
MEDICINE 48:8
Question 2
A 16-year old boy presented with toniceclonic seizures. On
further questioning, he and his mother noted that he was clumsy
in the mornings and often spilt his cereal.
Investigations revealed an abnormal EEG, and MRI showed a
large right-sided arachnoid cyst. He was then started on carba-
mazepine but his seizures got worse.
What is the most appropriate next step?
A. Refer him to neurosurgery for cyst removal to cure the
epilepsy
B. Start sodium valproate and wean him off carbamazepine
C. Add levetiracetam as a second agent
D. Measure the carbamazepine concentration to check
compliance with the medication
E. Explore psychological issues to see if some of the episodes
are dissociative
528 Ó 2020 Published by Elsevier Ltd.