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Epilepsy: mimics,
borderland and chameleons
Phil E M Smith

Correspondence to Abstract mimics, notably syncope and psycho-


Professor Phil E M Smith, Epilepsy mimics such as syncope and
Department of Neurology, The
genic attacks, can present like epilepsy,
psychogenic attacks, can present like epilepsy, and may be managed erroneously as
Epilepsy Unit, University Hospital
of Wales, Cardiff CF14 4XW, UK; and can be erroneously managed as epilepsy. epilepsy (often for the long term),
smithpe@cf.ac.uk There are also several conditions at the
yet clearly are distinct from it.
borderland that closely relate to epilepsy yet are
Received 10 April 2012 Furthermore, there are several condi-
probably separate from it, eg. migralepsy and
Accepted 5 August 2012
parasomnia. Finally, there are times when
tions closely relating to epilepsy that
epileptic seizures resemble one of the epilepsy are probably separate from epilepsy,
mimics. This is epilepsy in disguise—the epilepsy for example, migralepsy and parasom-
chameleons. Seizures with typically unusual nia: these are at the borderland of epi-
manifestations, such as occipital or parietal lobe lepsy. Finally, there are situations when
seizures, or those occurring in situations where epileptic seizures resemble one of the
another cause seems more likely, eg, in a person epilepsy mimics. This is epilepsy in
with alcoholism, may well be overlooked as disguise—an epilepsy chameleon.2
epilepsy and initially escape diagnosis. This Figure 1 shows the diagrammatic rela-
review explores the mimics of adult epilepsy, the tionship between epilepsy, its border-
epilepsy borderland, and focuses particularly on
land, its mimics and its chameleons.
epilepsy chameleons.
Note that epilepsy mimics are part of
Introduction other conditions’ chameleons list, for
The wide differential diagnosis of epi- example, of transient ischaemic
sodic altered consciousness presents a attacks, dementia, multiple sclerosis.
major diagnostic problem.1 Epilepsy Similarly, all epilepsy chameleons
appear on the lists of other conditions’
mimics (figure 2).
In practice, the labelling of episodic
loss of consciousness errs more
towards diagnosing epilepsy when it
is not, rather than failing to diagnose
epilepsy when it is. Thus, epilepsy
mimics are more problematic in prac-
tice than are epilepsy chameleons.
Nevertheless, our patients need us to
recognise and treat their epilepsy
promptly when it occurs, even if it
comes in disguise.
This review briefly explores mimics
of adult epilepsy, the epilepsy border-
land, and focuses particularly on epi-
lepsy chameleons. The main focus
here is in on adults: paediatric presen-
tations are more complex, with greater
propensity for misdiagnosis of parox-
ysmal events at either of the epilepsy
spectrum.

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test to monitor seizure frequency and severity—


equivalent to the ‘HbA1c’ in diabetes, there is no
alternative but to accept a patient’s report that there
have been, for example, three seizures in 6 months.
Some points in the history may be very
helpful in suggesting epilepsy: how the patient
tells the story;3 seizures clustering rather than
evenly spread out; and individual seizures being
stereotyped in character. Conversely, investiga-
tions may sometimes only muddy the water:
mimics are more often mislabelled as epilepsy
if undue weight is put upon a ‘positive’ EEG,
for example, photosensitivity or ‘epileptiform’
changes. The inter-ictal EEG is a great friend in
context, but a threat to well-being if seemingly
positive results are accorded power to overturn
a history-derived diagnosis. The three Cs of
EEG interpretation are ‘context, context and
Figure 1 Epilepsy: mimics, borderland and chameleons. context’.

Syncope
Epilepsy mimics Syncope is the most common cause of sudden
Syncope and psychogenic non-epileptic seizures loss of consciousness: most syncope is managed
comprise the main mimics of epilepsy; others are either in primary care or is referred to a cardiolo-
rare. The diagnosis of epilepsy is often incorrect, gist. Myoclonic jerks are well known to accom-
perhaps up to 20% of cases. The main reason is that pany syncope ( particularly following Lempert
epilepsy diagnosis relies largely on the history (and et al’s4 memorable study). Those giving wit-
witness account) rather than upon tests. Without a nessed accounts, often surprised and frightened
consistent diagnostic test (such as there is for dia- by the attack, will commonly overestimate how
betes), clinicians must accept that epilepsy manage- long such jerks last. When patients with syncope
ment is often founded upon likelihood rather present to a neurologist it is usually because they
than certainty. Although the inter-ictal EEG provides were thought first to have had a seizure. As a
additional information, it is rarely (in adults) suffi- result, neurologists see syncope mainly from the
cient alone to make the diagnosis. Also, without a severe end of a spectrum. These patients must be
considered carefully as a significant proportion
will have a cardiac (especially arrhythmogenic)
cause, which carries a high risk of sudden cardiac
death. On this basis discussions about the risk of
sudden unexplained death are perhaps more rele-
vant when the diagnosis is ‘unexplained loss of
consciousness’ than when the diagnosis is of
epilepsy.

Reflex syncope
Most transient loss of consciousness is reflex
(vasovagal) syncope, attributable to an overactive
autonomic nervous system in a young healthy
person. The classical tetrad (four Ps) of posture
(onset when upright), prodrome (blurring or
blacking of vision, nausea, light headedness and
sweating), provoking factors (sight of blood, pain
and bathroom) and prompt recovery are helpful
Figure 2 One condition’s mimic is another condition’s pointers, though none is diagnostic alone. Note
chameleon. that nausea at the onset reflects vagal over-

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Figure 3 Cardioinhibitory syncope during head-up tilt-table testing. The patient had been previously treated for epilepsy. At 20 min
into the tilt-table test, there was progressive bradycardia, culminating in cardiac arrest, with symptom reproduction; sinus rhythm
resumed on being lain flat.

activity, and so offers some reassurance as to the (lying for 3 min, then measuring blood pressure
benign nature of the blackout. Conversely, and pulse at 0, 3 and 5 min).
absence of nausea leaves cardiac syncope as an
option. Reflex syncope can take other forms, Cardiac syncope
sometimes very severe with cardioinhibition and Cardiac syncope often presents to neurologists as
convulsion (figure 3), sufficient convincingly to a first suspected seizure. Textbooks may highlight
mimic epilepsy. Other reflex syncopes have cardiac syncope as occurring on exertion; in
unusual provoking stimuli; for example, mictur- practice it more commonly presents as a sudden
ition, coughing, swallowing, laughing or orgasm. unheralded loss of consciousness with subsequent
Carotid sinus syncope, unusually for a reflex prompt and full recovery—the patient may
syncope, becomes more common with age: one recover sufficiently to send away the ambulance
theory is that the rigidity of the ageing carotid —or with convulsive seizures in sleep. Since
increases the carotid sinus movement resulting every such syncope represents an episode of
from a physical stimulus. cardiac arrest, their recognition is urgent.
The first priority is to risk stratify for sudden
Orthostatic syncope death.5 The most common and important cause
Presyncope and syncope that quickly follow is scar-related ventricular tachycardia: a previ-
standing suggest autonomic failure. The cause ously scarred myocardium providing the source
may be autonomic neuropathy (eg, elderly and of ventricular arrhythmia. Thus, the most
diabetes mellitus) or vasodilator medications (eg, important ECG finding in the emergency room
for hypertension). The characteristic feature on in an older person with unexplained blackout is
head-up tilt-table testing is a gradual fall in blood not of acute myocardial infarction but is of prior
pressure from the outset, without the usual com- myocardial infarction, notably pathological Q
pensatory rise in pulse rate. Thus, in patients waves. For the younger patient, the neurologist
with suspected orthostatic hypotension, lying (who will request a 12-lead ECG for all patients
and standing blood pressure measurement is with undiagnosed blackouts) also needs to recog-
helpful and worth spending a few minutes on nise several ECG patterns, notably hypertrophic

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cardiomyopathy, long QT syndrome, arrhythmo-


genic right ventricular cardiomyopathy, Brugada Box 1 Mimics of epilepsy
syndrome and Wolf-Parkinson-White syndrome.6
▸ Syncope
▸ Reflex
Psychogenic non-epileptic seizures – Vasovagal, micturition, swallow, carotid sinus, orgasmic
Psychogenic non-epileptic seizures (PNES) are an and laughing
important cause of apparently treatment-resistant ▸ Cardiac
epilepsy and remain a major diagnostic challenge – Arrhythmogenic
in epileptology. The two main PNES groups – Elderly: scar-related ventricular tachycardia
– Young: long QT syndrome, short QT syndrome, arrhyth-
are panic disorder (also occurring as a reaction mogenic right ventricular cardiomyopathy
in people with epilepsy) and dissociative – Structural, aortic stenosis, hypertrophic cardiomyopathy
disorder (‘pseudoseizure’), often developing in ▸ Orthostatic
patients with no history of epilepsy. The main – Autonomic failure
markers distinguishing PNES from epileptic ▸ Psychogenic non-epileptic attack disorder
– Panic disorder (especially in people with epilepsy)
seizures are:
– Dissociative
• the way the patient tells the story (not focusing on – Factitious and malingering
the seizure symptoms, avoids using the word ▸ Sleep disorders
‘seizure’, etc);3 – Narcolepsy syndrome and cataplexy
• that they are prolonged (many minutes); – Parasomnias (see Borderland of epilepsy section)
▸ Paroxysmal symptoms of structural brain disease
• associated with hyperventilation and eyes closed;
– Multiple sclerosis
and that they present as treatment-resistant epilepsy – Tumour, eg, brainstem glioma
despite an often normal intellect and brain imaging. ▸ Vascular
Note that patients with PNES may bite their – Migraine (hemiparetic, occipital, ‘basilar artery’)
tongue (though usually the front not the side), – Shaking transient ischaemic attack (critical bilateral
may injure themselves (though usually cuts, carpet stenosis)
burns or wrist injury from falling on to an out- – Subclavian steal syndrome
– Moyamoya (combination of TIA and seizures)
stretched arm) and may report seizures from sleep – Not vertebrobasilar insufficiency
(the night time being a vulnerable time for panic ▸ Hypoglycaemia
symptoms and likely to be awake at the onset). – Behaviour disturbance
– Hemiparesis
Rarer epilepsy mimics ▸ Movement disorder
– Paroxysmal kinesigenic dystonia/dyskinesia
Some less common epilepsy mimics are outlined – Myoclonus following hypoxia
in box 1 and have been reviewed in detail ▸ Hydrocephalus
elsewhere.7 – Colloid cyst
– Chiari malformation
Borderland of epilepsy ▸ Drop attacks
– Postural instability
Gowers8 coined the term ‘the borderland of epi-
– Psychogenic
lepsy’ in 1907 to describe a group of conditions
closely related to epilepsy: ‘faints, vagal attacks,
vertigo, migraine and sleep symptoms’. Although
may not always be obvious, even in video-EEG-
reflex (vasovagal) syncope and most forms of
recorded episodes.
vertigo can now clearly be separated from epi-
lepsy, migralepsy, parasomnias and startle syn-
dromes remain firmly where Gowers first Non-REM parasomnias
positioned them—‘near it, but not of it’.9 The Parasomnias arising from non-REM sleep include
treatment of conditions at the borderland confusional arousals, periodic limb movements,
overlap with epilepsy (eg, clonazepam for rhythmic movement disorder, night terrors and
parasomnia and topiramate for migralepsy) but somnambulism: all easily confused with seizures.
the social implications are very different, for Table 1 shows the clinical features that help to
example, for driving eligibility and social stigma. distinguish parasomnias from epilepsy.
Medications such as clonazepam may help both
Parasomnias conditions. Patients with ‘familial parasomnia’
Parasomnias clearly overlap with frontal lobe epi- are perhaps particularly likely actually to have
leptic seizures, and their distinction from epilepsy frontal lobe epilepsy.

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Table 1 Frontal lobe seizures versus parasomnias: clinical and leukoencephalopathy) appear particularly
pointers prone to developing migraine coma.
Frontal lobe seizures Parasomnias
Startle syndromes
From sleep or awake From sleep
Onset in childhood or Onset in childhood (can persist to adult)
Startle syndromes are rare and occur usually in
adult babies and young children, manifesting as a phys-
Stereotyped Variable ical startle response to a loud or intense stimulus.
Short: up to 1 min Longer: several minutes Startle syndrome diagnosis depends on clinical
Frequent, eg, many per Infrequent, for example, once per night history, electromyographic studies and genetic
night screening. There are three main groups.11
Clustering Isolated
Any time in sleep Early in sleep (NREM parasomnia) late in Hyperekplexia.
sleep (REM parasomnia)
1. ‘Major’ hyperekplexia is a genetic disorder (with
No amnesia (often retain Amnesia (but may recall dream from mutations in the α1 subunit of the glycine receptor
awareness) REM-sleep behaviour disorder)
gene, GLRA1), presenting in the neonatal period
with continuous stiffness and includes excessive
REM parasomnias startle and startle-induced falls. Milder forms pre-
REM sleep behaviour disorder results from dis- senting later may be mislabelled as stiff-person
sociation between REM sleep and axial atonia— syndrome.
without this loss of tone the patients physically 2. ‘Minor’ hyperekplexia, of unknown cause, where
act out their dreams. It is usually of elderly there is excessive startle without stiffness. It may
onset, and associated with brainstem disease, and be mislabelled as non-organic.
may predict later onset of idiopathic Parkinson’s
disease. Injury may result to self and others. Neuropsychiatric startle disorders
Clonazepam is usually effective. In these conditions, behavioural features accom-
pany excessive startling.
Migraine
Startle-induced epilepsy
There are two groups of migraine overlap This is considered as an epilepsy ‘chameleon’
syndromes. (see Chameleons section).
Migralepsy
Other reflex phenomena
Migraine and epilepsy have many clinical over-
laps. Patients with migraine (especially with aura) Some non-epileptic reflex phenomena may rarely
may report transient atypical symptoms during present to neurologists. Photic sneezing, is a
episodes, such as depersonalisation or even loss common familial trait where sneezing results
of consciousness, which overlap with (occipital) from exposure to bright (though not necessarily
seizures. Conversely, people with epilepsy may flashing) lights.
report migraine-type headache following sei-
zures. Antiepileptic medications often prove Chameleons
effective prophylaxis for migraine. Seizures that resemble mimics more than seizures
Clinicians may use the term migralepsy10 to risk being mislabelled. There are several reasons,
describe cases where there is clear overlap. The discussed below, as to why an epileptic seizure
2004 International Classification for Headache may be misdiagnosed. Perhaps the most important
Disorders (ICHD-II) proposed two diagnostic cri- distinguishing feature is that seizures are typically
teria for migralepsy: (A) migraine fulfilling criteria the highly stereotyped whereas events that are not
for migraine with aura and (B) a seizure fulfilling seizures tend to show more variation. A corollary
diagnostic criteria for one type of epileptic attack, of this is that a diagnosis may become clearer with
occurring less than 1 h after a migraine aura. follow-up if further events occur—which may
demonstrate the highly stereotyped nature of
Migraine syncope events.
Migraine syncope typically manifests as migraine-
type symptoms followed by gradual onset (over Seizures with unusual phenotypes
many minutes) into loss of consciousness. Seizures arising from certain parts of the brain
Patients with CADASIL (cerebral autosomal- may show ‘atypical’ features, misleading the clin-
dominant arteriopathy with subcortical infarcts ician into missing the epileptic aetiology. This is

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especially likely if seizures remain localised rather nature. Very minor symptoms, such as déjà vu,
than going onto secondarily generalisation. This epigastric aura or auditory aura, particularly if
is more likely in patients with intellectual disabil- there is retained awareness, are easily dismissed
ity where symptom description may be less clear. (by patient and doctor) as a normal character
Furthermore, EEG can be normal between and trait. In practice, such ‘aura’ symptoms are often
even during events (common if a seizure focus is only diagnosed retrospectively after a tonic-clonic
deep-seated). There are examples of ‘atypical’ seizure. There are several situations where mis-
seizure types arising from all lobes of the brain. diagnosis is more likely:
1. Ictal fear, accompanied by palpitation and tachy-
Generalised-onset seizures cardia, is easily labelled as panic disorder.
Idiopathic (genetic) generalised epilepsies mani- Occasionally, ictal fear may trigger a psychogenic
festing only as minor seizures (absences or myo- non-epileptic response as the main manifestation
clonus)—at least until generalised tonic-clonic of the event, only adding to the diagnostic
seizures occur—may not be recognised as confusion.
epilepsy. 2. Ictal bradycardia, accompanying temporal lobe sei-
1. Absence seizures may be dismissed (by patients, zures, manifests as a brief aura (epigastric or déjà
parents, teachers and doctors) as daydreaming and vu) followed by syncope (with pallor and sweating)
poor concentration, with consequent detriment to as the dominant feature. Many such patients
school performance. acquire a permanent pacemaker before seeing a
2. Myoclonic jerks of limbs or head, even if provoked neurologist.
by flashing lights, may initially be labelled as a 3. Transient epileptic amnesia, with recurrent antero-
character trait, a tic or as psychogenic. grade memory loss and repeated questioning,
3. Eyelid myoclonia are easily mistaken for behav- lasting often many minutes or even an hour, may
ioural habit spasms if associated altered awareness easily be confused with transient global amnesia
is only minimal or not recognised. (although this is typically a one-off, with duration
of several hours).
4. Ictal vomiting may be the dominant manifestation
Frontal lobe seizures of temporal lobe epilepsy and can be diagnosed
The large size of the frontal lobe underlies its initially (and especially in the learning disabled) as
broad spectrum of seizure phenotype. Frontal gastrointestinal upset.
complex partial seizures arising from the supple- 5. Ictal spitting is an unusual seizure manifestation
mentary motor area on the medial surface of the that suggests a non-dominant (right-sided) tem-
frontal lobe typically arise from sleep, often poral lobe focus, and is often labelled as behav-
many times per night, and may be surprisingly ioural or psychogenic.12
brief and with some retained awareness. 6. Laryngeal spasm typically arises from the insular
1. Hypermotor seizures, limited to agitation, vocalisa- region, and is easily misdiagnosed as psychogenic.
tions and aggression may easily be mislabelled as
parasomnia; those with bizarre posturing, back
arching, limb cycling risk, hyperventilation, Parietal lobe seizures
retained awareness and extreme fear being labelled Parietal lobe seizures are rare, though they may
as REM-sleep behaviour disorder or psychogenic be under-recognised. The risk of misdiagnosis is
non-epileptic seizures. Moreover, the ictal EEG increased by the sometimes bizarre nature of the
may not show the expected midline spikes because
symptoms, the lack of visible motor manifesta-
of the deep-seated, localised seizure focus that may
not show on scalp EEG.
tions and the often normal EEG even during
2. Autosomal-dominant nocturnal frontal lobe epi- events. The patient’s distress may be com-
lepsy does manifest as repeated localised posturing pounded by the retained awareness during
without altered awareness and arising from sleep, unpleasant symptoms, the delay in diagnosis
and was for years considered to be a parasomnia and the implications of a psychogenic cause.
or even as a primary movement disorder (it was A common underlying cause is low-grade glioma,
long classified as ‘paroxysmal nocturnal dystonia’), or alternatively ullegyria (figure 4) from ‘border
its epileptic nature easily passing unnoticed. zone’ infarction in infancy (and hence the
importance of a birth history in epilepsy clinics).
Temporal lobe epilepsy Ullegyria typically affects the underlying white
This is the most common form of focal-onset matter (vulnerable to hypotensive infarction)
adult epilepsy, with many manifestations, often more than the overlying grey matter ( partially
with the risk of overlooking their epileptic protected by the greater number of collaterals).

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Figure 4 Ullegyria. MR brain scan (coronal T1-weighted)


showing ullegyria, with atrophy more marked deep in sulci
rather than superficially on gyri.

The main manifestations of parietal lobe seizures


are:
1. Ictal pain, manifesting as an intermittent focal
pain syndrome.
2. Non-specific sensory symptoms, including tingling,
numbness and feelings of unilateral body tightness,
which may be labelled as migraine with sensory Figure 5 (A) Monocular polyopia, as described by a patient
symptoms. with a right-sided (non-dominant) occipital epilepsy. (B)
3. Perception difficulty intermittently, is easily Palinopsia (visual perseveration) in a patient with cerebral
labelled as non-specific or psychological. infiltration of non-Hodgkin’s lymphoma in whom the image of
a knee X-ray became temporarily incorporated into his vision
(reproduced from Lancet 2003;361:1098, with permission).
Occipital epilepsy
Occipital seizure symptoms may seem bizarre
and are particularly likely to be overlooked or child or teenager being considered to have a psy-
misdiagnosed as something other than epilepsy. chogenic problem.
They occur more commonly in children, and so 3. Palinopsia ( palin=again) is where a visual stimulus
adult neurologists may be less used to hearing leads to abnormal visual persistence, with the illu-
and interpreting such histories. Occipital seizures sion either becoming incorporated into vision or
manifesting as multiple images (figure 5A,B). It is
have several manifestations:
not surprising that such a bizarre symptom should
1. Positive visual auras may be misdiagnosed as
commonly be dismissed as functional.
migraine. Migraine visual auras, however, are typic-
4. Blinking is a common accompaniment of occipital
ally monochrome and linear, with zigzags shaped
epilepsy, but again with the retained awareness,
like the aerial view of a town wall (‘teichopsia’ or for-
can seem to be psychological.
tification spectra), whereas occipital epilepsy auras
5. Migralepsy is considered above under Borderland
are typically coloured shapes or even formed objects.
of epilepsy section.
However, 5–10% of occipital seizures have no visual
component, but spread rapidly to the temporal and
frontal lobes, obscuring their occipital origin. Hypothalamic seizures
2. Ictal blindness is not widely known as a seizure Seizures resulting from a hypothalamic hamar-
manifestation, particularly among adult physicians. toma may manifest (usually in children) as epi-
When it continues for many minutes and with sodes of unprovoked giggling or laughing
retained awareness as often happens, may lead to a (gelastic seizures). The MRI changes are subtle,

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even in specialist hands, and will be missed Seizures where mimics are more likely
unless is specifically sought. However, only half Special situations
of gelastic seizures arise from the hypothalamus: Loss of consciousness in certain situations may
half arise from the insular region. imply diagnoses other than epilepsy.
1. Seizures in the bathroom, a restaurant, and the
Brainstem and cerebellar seizures doctors’ surgery, prompt the likely diagnosis of
Occasional infants with cerebellar gangliogliomas syncope ( provoked by posture, heat, sight of
and ‘hemifacial spasm’ have had a proven diag- blood, etc).
nosis of ‘cerebellar epilepsy’. Cerebellar epilepsy 2. Seizures on a psychiatric ward or in patients with
has not been reported in adults. strong psychiatric history prompt initial suspicion
of psychogenic non-epileptic attacks.
Non-convulsive status epilepticus 3. Seizures on a cardiac ward may be understandably
Complex partial status epilepticus is an important suspected first as having had cardiac syncope.
treatable cause of abrupt onset of confusion 4. Seizures on an intensive care unit may sometimes
be first attributed to movement disorder associated
and/or subacute dementia. It may develop de
with either metabolic disturbance or hypoxic-
novo, but usually accompanies an acute brain ischaemic encephalopathy.
insult, for example, viral encephalitis or venous
sinus thrombosis. There may be only very minor Seizures accompanying existing conditions
motor manifestations and even the EEG changes Some clinical situations are so dominated by
may be subtle: it is easily dismissed as being associated features that epileptic seizures can be
part of the underlying disease, or mislabelled, overlooked.
for example, as immune encephalitis such 1. Psychiatric history: Seizures in a person with
as N-methyl D-aspartate (NMDA)-associated chronic anxiety, self-harm, drug addiction, dyscon-
encephalitis or Creutzfeldt-Jakob disease. trol (eg, following previous head injury) risk,
despite their increased risk of epilepsy, being
Reflex epilepsies labelled as psychogenic episodes.
Reflex seizures, including photosensitivity, com- 2. Learning disability: Seizures, particularly of
prise up to 9% of epileptic seizures.13 Various complex partial (dyscognitive) type in someone
sensory and emotional stimuli may provoke sei- with significant intellectual disability, may easily be
zures, notably light and music. Photosensitive labelled as a behavioural disturbance only.
epilepsy is well known and hugely over- 3. Neurodegenerative disease: Seizures in patients
diagnosed by patients—many of whom habitually with Alzheimer’s disease or Huntington’s disease
but unnecessarily avoid flashing lights—and so (eg, blank spells or automatism) may be ascribed
true photosensitivity rarely escapes diagnosis. to movement disorder or behaviour disturbance.
Seizures as a reflex response to other phenom-
ena are less well known. Examples include
pattern-sensitive seizures (which, if occurring Spontaneous seizures where acute symptomatic seizures
are more likely
without photosensitivity, may initially seem suffi-
1. Diabetes mellitus, with previous hypoglycaemic
ciently strange to be overlooked as epilepsy) and
episodes, may lead to subsequent sleep-related sei-
reading epilepsy (lower lip tremor building over zures being too easily attributed to hypoglycaemia.
many minutes of reading and culminating in a This mislabelling sometimes persists despite docu-
generalised tonic-clonic seizure). Some provoking mented normal ictal plasma glucose levels.
factors for seizures might initially seem just too 2. Alcoholism, with previous alcohol withdrawal sei-
bizarre to be true: eating, tooth brushing, hot zures, may delay the diagnosis (and management
water (especially as a genetic trait in India), mic- of ) epilepsy, with seizures being presumed due to
turition, and emotionally triggered seizures.14 alcohol withdrawal.
Sexual activity may rarely triggers epileptic sei- 3. Illicit drug use, for example of cocaine or intraven-
zures (orgasmic epilepsy): case reports suggest ous drugs, may prompt the clinician to think first
that this occurs mainly in women and mostly of psychogenic non-epileptic seizures or drug with-
localises to the right hemisphere on inter-ictal drawal seizures, rather than epilepsy.
EEG. Startle-induced epilepsy is rare (considered
under Borderland of epilepsy section), and mani- Seizures in rare conditions
fests as seizures provoked by startle phenomena Some rarely encountered conditions may present
in genetically susceptible children. with seizures but, because of other manifestations,

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the seizures may be mislabelled and the under- less of a problem that often needs clarifying.
lying condition remain undiagnosed. A further group of conditions lie at the border-
1. Autoimmune encephalitis: The facio-brachial dys- land between epilepsy and ‘not epilepsy’, the
tonic seizures characteristically preceding limbic so-called borderland of epilepsy, where better
encephalitis due to voltage-gated potassium understanding of the pathophysiolgy will eventu-
channel-complex-antibody (VGKC-complex-Ab) ally clarify the cause.
manifest as brief (a few seconds) and frequent
This paper was reviewed by Mark Manford, Cambridge, UK.
(eg, 50 per day) dystonic seizures, easily be mis-
labelled in the context of behavioural disturbance Competing interests None.
and memory loss, especially as they are typically Provenance and peer review Commissioned: externally peer-
resistant to antiepileptic medication (though reviewed.
responsive to immunosuppression).15
2. Acute intermittent porphyria: Patients with seizures
caused by porphyria may have these mislabelled as References
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Philadelphia: P. Blakiston’s Son, 1907.
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