Article Text
Abstract
Epilepsy mimics such as syncope and psychogenic attacks, can present like epilepsy, and can be erroneously managed as epilepsy. There are also several conditions at the borderland that closely relate to epilepsy yet are probably separate from it, eg. migralepsy and parasomnia. Finally, there are times when epileptic seizures resemble one of the epilepsy mimics. This is epilepsy in disguise–the epilepsy chameleons. Seizures with typically unusual manifestations, such as occipital or parietal lobe seizures, or those occurring in situations where another cause seems more likely, eg, in a person with alcoholism, may well be overlooked as epilepsy and initially escape diagnosis. This review explores the mimics of adult epilepsy, the epilepsy borderland, and focuses particularly on epilepsy chameleons.
- Epilepsy
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Introduction
The wide differential diagnosis of episodic altered consciousness presents a major diagnostic problem.1 Epilepsy mimics, notably syncope and psychogenic attacks, can present like epilepsy, and may be managed erroneously as epilepsy (often for the long term), yet clearly are distinct from it. Furthermore, there are several conditions closely relating to epilepsy that are probably separate from epilepsy, for example, migralepsy and parasomnia: these are at the borderland of epilepsy. Finally, there are situations when epileptic seizures resemble one of the epilepsy mimics. This is epilepsy in disguise—an epilepsy chameleon.2 Figure 1 shows the diagrammatic relationship between epilepsy, its borderland, its mimics and its chameleons. Note that epilepsy mimics are part of other conditions’ chameleons list, for example, of transient ischaemic attacks, dementia, multiple sclerosis. 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 practice 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 borderland, and focuses particularly on epilepsy chameleons. The main focus here is in on adults: paediatric presentations are more complex, with greater propensity for misdiagnosis of paroxysmal events at either of the epilepsy spectrum.
Epilepsy mimics
Syncope and psychogenic non-epileptic seizures comprise the main mimics of epilepsy; others are rare. The diagnosis of epilepsy is often incorrect, perhaps up to 20% of cases. The main reason is that epilepsy diagnosis relies largely on the history (and witness account) rather than upon tests. Without a consistent diagnostic test (such as there is for diabetes), clinicians must accept that epilepsy management is often founded upon likelihood rather than certainty. Although the inter-ictal EEG provides additional information, it is rarely (in adults) sufficient alone to make the diagnosis. Also, without a 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, investigations 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 context’.
Syncope
Syncope is the most common cause of sudden loss of consciousness: most syncope is managed either in primary care or is referred to a cardiologist. Myoclonic jerks are well known to accompany syncope (particularly following Lempert et al's4 memorable study). Those giving witnessed accounts, often surprised and frightened by the attack, will commonly overestimate how long such jerks last. When patients with syncope present to a neurologist it is usually because they were thought first to have had a seizure. As a result, neurologists see syncope mainly from the 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 relevant 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 pointers, though none is diagnostic alone. Note that nausea at the onset reflects vagal over-activity, and so offers some reassurance as to the benign nature of the blackout. Conversely, absence of nausea leaves cardiac syncope as an option. Reflex syncope can take other forms, sometimes very severe with cardioinhibition and convulsion (figure 3), sufficient convincingly to mimic epilepsy. Other reflex syncopes have unusual provoking stimuli; for example, micturition, coughing, swallowing, laughing or orgasm. Carotid sinus syncope, unusually for a reflex syncope, becomes more common with age: one theory is that the rigidity of the ageing carotid increases the carotid sinus movement resulting from a physical stimulus.
Orthostatic syncope
Presyncope and syncope that quickly follow standing suggest autonomic failure. The cause may be autonomic neuropathy (eg, elderly and diabetes mellitus) or vasodilator medications (eg, for hypertension). The characteristic feature on head-up tilt-table testing is a gradual fall in blood pressure from the outset, without the usual compensatory rise in pulse rate. Thus, in patients with suspected orthostatic hypotension, lying and standing blood pressure measurement is helpful and worth spending a few minutes on (lying for 3 min, then measuring blood pressure and pulse at 0, 3 and 5 min).
Cardiac syncope
Cardiac syncope often presents to neurologists as a first suspected seizure. Textbooks may highlight cardiac syncope as occurring on exertion; in practice it more commonly presents as a sudden unheralded loss of consciousness with subsequent prompt and full recovery—the patient may recover sufficiently to send away the ambulance—or with convulsive seizures in sleep. Since every such syncope represents an episode of cardiac arrest, their recognition is urgent.
The first priority is to risk stratify for sudden death.5 The most common and important cause is scar-related ventricular tachycardia: a previously scarred myocardium providing the source of ventricular arrhythmia. Thus, the most important ECG finding in the emergency room in an older person with unexplained blackout is not of acute myocardial infarction but is of prior myocardial infarction, notably pathological Q waves. For the younger patient, the neurologist (who will request a 12-lead ECG for all patients with undiagnosed blackouts) also needs to recognise several ECG patterns, notably hypertrophic cardiomyopathy, long QT syndrome, arrhythmogenic right ventricular cardiomyopathy, Brugada syndrome and Wolf-Parkinson-White syndrome.6
Psychogenic non-epileptic seizures
Psychogenic non-epileptic seizures (PNES) are an important cause of apparently treatment-resistant epilepsy and remain a major diagnostic challenge in epileptology. The two main PNES groups are panic disorder (also occurring as a reaction in people with epilepsy) and dissociative disorder (‘pseudoseizure’), often developing in patients with no history of epilepsy. The main markers distinguishing PNES from epileptic seizures are:
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the way the patient tells the story (not focusing on the seizure symptoms, avoids using the word ‘seizure’, etc);3
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that they are prolonged (many minutes);
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associated with hyperventilation and eyes closed; and that they present as treatment-resistant epilepsy despite an often normal intellect and brain imaging.
Note that patients with PNES may bite their tongue (though usually the front not the side), may injure themselves (though usually cuts, carpet burns or wrist injury from falling on to an outstretched arm) and may report seizures from sleep (the night time being a vulnerable time for panic symptoms and likely to be awake at the onset).
Rarer epilepsy mimics
Some less common epilepsy mimics are outlined in box 1 and have been reviewed in detail elsewhere.7
Mimics of epilepsy
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Syncope
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Reflex
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Vasovagal, micturition, swallow, carotid sinus, orgasmic and laughing
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Cardiac
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Arrhythmogenic
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Elderly: scar-related ventricular tachycardia
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Young: long QT syndrome, short QT syndrome, arrhythmogenic right ventricular cardiomyopathy
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Structural, aortic stenosis, hypertrophic cardiomyopathy
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Orthostatic
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Autonomic failure
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Psychogenic non-epileptic attack disorder
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Panic disorder (especially in people with epilepsy)
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Dissociative
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Factitious and malingering
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Sleep disorders
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Narcolepsy syndrome and cataplexy
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Parasomnias (see Borderland of epilepsy section)
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Paroxysmal symptoms of structural brain disease
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Multiple sclerosis
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Tumour, eg, brainstem glioma
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Vascular
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Migraine (hemiparetic, occipital, ‘basilar artery’)
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Shaking transient ischaemic attack (critical bilateral stenosis)
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Subclavian steal syndrome
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Moyamoya (combination of TIA and seizures)
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Not vertebrobasilar insufficiency
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Hypoglycaemia
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Behaviour disturbance
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Hemiparesis
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Movement disorder
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Paroxysmal kinesigenic dystonia/dyskinesia
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Myoclonus following hypoxia
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Hydrocephalus
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Colloid cyst
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Chiari malformation
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Drop attacks
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Postural instability
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Psychogenic
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Borderland of epilepsy
Gowers8 coined the term ‘the borderland of epilepsy’ in 1907 to describe a group of conditions closely related to epilepsy: ‘faints, vagal attacks, vertigo, migraine and sleep symptoms’. Although reflex (vasovagal) syncope and most forms of vertigo can now clearly be separated from epilepsy, migralepsy, parasomnias and startle syndromes remain firmly where Gowers first positioned them—‘near it, but not of it’.9 The treatment of conditions at the borderland overlap with epilepsy (eg, clonazepam for parasomnia and topiramate for migralepsy) but the social implications are very different, for example, for driving eligibility and social stigma.
Parasomnias
Parasomnias clearly overlap with frontal lobe epileptic seizures, and their distinction from epilepsy may not always be obvious, even in video-EEG-recorded episodes.
Non-REM parasomnias
Parasomnias arising from non-REM sleep include confusional arousals, periodic limb movements, rhythmic movement disorder, night terrors and somnambulism: all easily confused with seizures. Table 1 shows the clinical features that help to distinguish parasomnias from epilepsy. Medications such as clonazepam may help both conditions. Patients with ‘familial parasomnia’ are perhaps particularly likely actually to have frontal lobe epilepsy.
REM parasomnias
REM sleep behaviour disorder results from dissociation between REM sleep and axial atonia—without this loss of tone the patients physically act out their dreams. It is usually of elderly onset, and associated with brainstem disease, and may predict later onset of idiopathic Parkinson's disease. Injury may result to self and others. Clonazepam is usually effective.
Migraine
There are two groups of migraine overlap syndromes.
Migralepsy
Migraine and epilepsy have many clinical overlaps. Patients with migraine (especially with aura) may report transient atypical symptoms during episodes, such as depersonalisation or even loss of consciousness, which overlap with (occipital) seizures. Conversely, people with epilepsy may report migraine-type headache following seizures. Antiepileptic medications often prove effective prophylaxis for migraine.
Clinicians may use the term migralepsy10 to describe cases where there is clear overlap. The 2004 International Classification for Headache Disorders (ICHD-II) proposed two diagnostic criteria for migralepsy: (A) migraine fulfilling criteria for migraine with aura and (B) a seizure fulfilling diagnostic criteria for one type of epileptic attack, occurring less than 1 h after a migraine aura.
Migraine syncope
Migraine syncope typically manifests as migraine-type symptoms followed by gradual onset (over many minutes) into loss of consciousness. Patients with CADASIL (cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy) appear particularly prone to developing migraine coma.
Startle syndromes
Startle syndromes are rare and occur usually in babies and young children, manifesting as a physical startle response to a loud or intense stimulus. Startle syndrome diagnosis depends on clinical history, electromyographic studies and genetic screening. There are three main groups.11
Hyperekplexia.
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‘Major’ hyperekplexia is a genetic disorder (with mutations in the α1 subunit of the glycine receptor gene, GLRA1), presenting in the neonatal period with continuous stiffness and includes excessive startle and startle-induced falls. Milder forms presenting later may be mislabelled as stiff-person syndrome.
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‘Minor’ hyperekplexia, of unknown cause, where there is excessive startle without stiffness. It may be mislabelled as non-organic.
Neuropsychiatric startle disorders
In these conditions, behavioural features accompany excessive startling.
Startle-induced epilepsy
This is considered as an epilepsy ‘chameleon’ (see Chameleons section).
Other reflex phenomena
Some non-epileptic reflex phenomena may rarely present to neurologists. Photic sneezing, is a common familial trait where sneezing results from exposure to bright (though not necessarily flashing) lights.
Chameleons
Seizures that resemble mimics more than seizures risk being mislabelled. There are several reasons, discussed below, as to why an epileptic seizure may be misdiagnosed. Perhaps the most important distinguishing feature is that seizures are typically the highly stereotyped whereas events that are not seizures tend to show more variation. A corollary of this is that a diagnosis may become clearer with follow-up if further events occur—which may demonstrate the highly stereotyped nature of events.
Seizures with unusual phenotypes
Seizures arising from certain parts of the brain may show ‘atypical’ features, misleading the clinician into missing the epileptic aetiology. This is especially likely if seizures remain localised rather than going onto secondarily generalisation. This is more likely in patients with intellectual disability where symptom description may be less clear. Furthermore, EEG can be normal between and even during events (common if a seizure focus is deep-seated). There are examples of ‘atypical’ seizure types arising from all lobes of the brain.
Generalised-onset seizures
Idiopathic (genetic) generalised epilepsies manifesting only as minor seizures (absences or myoclonus)—at least until generalised tonic-clonic seizures occur—may not be recognised as epilepsy.
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Absence seizures may be dismissed (by patients, parents, teachers and doctors) as daydreaming and poor concentration, with consequent detriment to school performance.
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Myoclonic jerks of limbs or head, even if provoked by flashing lights, may initially be labelled as a character trait, a tic or as psychogenic.
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Eyelid myoclonia are easily mistaken for behavioural habit spasms if associated altered awareness is only minimal or not recognised.
Frontal lobe seizures
The large size of the frontal lobe underlies its broad spectrum of seizure phenotype. Frontal complex partial seizures arising from the supplementary motor area on the medial surface of the frontal lobe typically arise from sleep, often many times per night, and may be surprisingly brief and with some retained awareness.
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Hypermotor seizures, limited to agitation, vocalisations and aggression may easily be mislabelled as parasomnia; those with bizarre posturing, back arching, limb cycling risk, hyperventilation, retained awareness and extreme fear being labelled as REM-sleep behaviour disorder or psychogenic non-epileptic seizures. Moreover, the ictal EEG may not show the expected midline spikes because of the deep-seated, localised seizure focus that may not show on scalp EEG.
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Autosomal-dominant nocturnal frontal lobe epilepsy does manifest as repeated localised posturing without altered awareness and arising from sleep, and was for years considered to be a parasomnia or even as a primary movement disorder (it was long classified as ‘paroxysmal nocturnal dystonia’), its epileptic nature easily passing unnoticed.
Temporal lobe epilepsy
This is the most common form of focal-onset adult epilepsy, with many manifestations, often with the risk of overlooking their epileptic nature. Very minor symptoms, such as déjà vu, epigastric aura or auditory aura, particularly if there is retained awareness, are easily dismissed (by patient and doctor) as a normal character trait. In practice, such ‘aura’ symptoms are often only diagnosed retrospectively after a tonic-clonic seizure. There are several situations where misdiagnosis is more likely:
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Ictal fear, accompanied by palpitation and tachycardia, is easily labelled as panic disorder. Occasionally, ictal fear may trigger a psychogenic non-epileptic response as the main manifestation of the event, only adding to the diagnostic confusion.
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Ictal bradycardia, accompanying temporal lobe seizures, manifests as a brief aura (epigastric or déjà vu) followed by syncope (with pallor and sweating) as the dominant feature. Many such patients acquire a permanent pacemaker before seeing a neurologist.
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Transient epileptic amnesia, with recurrent anterograde memory loss and repeated questioning, lasting often many minutes or even an hour, may easily be confused with transient global amnesia (although this is typically a one-off, with duration of several hours).
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Ictal vomiting may be the dominant manifestation of temporal lobe epilepsy and can be diagnosed initially (and especially in the learning disabled) as gastrointestinal upset.
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Ictal spitting is an unusual seizure manifestation that suggests a non-dominant (right-sided) temporal lobe focus, and is often labelled as behavioural or psychogenic.12
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Laryngeal spasm typically arises from the insular region, and is easily misdiagnosed as psychogenic.
Parietal lobe seizures
Parietal lobe seizures are rare, though they may be under-recognised. The risk of misdiagnosis is increased by the sometimes bizarre nature of the symptoms, the lack of visible motor manifestations and the often normal EEG even during events. The patient's distress may be compounded by the retained awareness during unpleasant symptoms, the delay in diagnosis and the implications of a psychogenic cause. A common underlying cause is low-grade glioma, or alternatively ullegyria (figure 4) from ‘border zone’ infarction in infancy (and hence the importance of a birth history in epilepsy clinics). Ullegyria typically affects the underlying white matter (vulnerable to hypotensive infarction) more than the overlying grey matter (partially protected by the greater number of collaterals). The main manifestations of parietal lobe seizures are:
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Ictal pain, manifesting as an intermittent focal pain syndrome.
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Non-specific sensory symptoms, including tingling, numbness and feelings of unilateral body tightness, which may be labelled as migraine with sensory symptoms.
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Perception difficulty intermittently, is easily labelled as non-specific or psychological.
Occipital epilepsy
Occipital seizure symptoms may seem bizarre and are particularly likely to be overlooked or misdiagnosed as something other than epilepsy. They occur more commonly in children, and so adult neurologists may be less used to hearing and interpreting such histories. Occipital seizures have several manifestations:
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Positive visual auras may be misdiagnosed as migraine. Migraine visual auras, however, are typically monochrome and linear, with zigzags shaped like the aerial view of a town wall (‘teichopsia’ or fortification spectra), whereas occipital epilepsy auras are typically coloured shapes or even formed objects. However, 5–10% of occipital seizures have no visual component, but spread rapidly to the temporal and frontal lobes, obscuring their occipital origin.
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Ictal blindness is not widely known as a seizure manifestation, particularly among adult physicians. When it continues for many minutes and with retained awareness as often happens, may lead to a child or teenager being considered to have a psychogenic problem.
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Palinopsia (palin=again) is where a visual stimulus leads to abnormal visual persistence, with the illusion either becoming incorporated into vision or manifesting as multiple images (figure 5A,B). It is not surprising that such a bizarre symptom should commonly be dismissed as functional.
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Blinking is a common accompaniment of occipital epilepsy, but again with the retained awareness, can seem to be psychological.
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Migralepsy is considered above under Borderland of epilepsy section.
Hypothalamic seizures
Seizures resulting from a hypothalamic hamartoma may manifest (usually in children) as episodes of unprovoked giggling or laughing (gelastic seizures). The MRI changes are subtle, even in specialist hands, and will be missed unless is specifically sought. However, only half of gelastic seizures arise from the hypothalamus: half arise from the insular region.
Brainstem and cerebellar seizures
Occasional infants with cerebellar gangliogliomas and ‘hemifacial spasm’ have had a proven diagnosis of ‘cerebellar epilepsy’. Cerebellar epilepsy has not been reported in adults.
Non-convulsive status epilepticus
Complex partial status epilepticus is an important treatable cause of abrupt onset of confusion and/or subacute dementia. It may develop de novo, but usually accompanies an acute brain insult, for example, viral encephalitis or venous sinus thrombosis. There may be only very minor motor manifestations and even the EEG changes may be subtle: it is easily dismissed as being part of the underlying disease, or mislabelled, for example, as immune encephalitis such as N-methyl d-aspartate (NMDA)-associated encephalitis or Creutzfeldt-Jakob disease.
Reflex epilepsies
Reflex seizures, including photosensitivity, comprise up to 9% of epileptic seizures.13 Various sensory and emotional stimuli may provoke seizures, notably light and music. Photosensitive epilepsy is well known and hugely over-diagnosed by patients—many of whom habitually but unnecessarily avoid flashing lights—and so true photosensitivity rarely escapes diagnosis.
Seizures as a reflex response to other phenomena are less well known. Examples include pattern-sensitive seizures (which, if occurring without photosensitivity, may initially seem sufficiently strange to be overlooked as epilepsy) and reading epilepsy (lower lip tremor building over many minutes of reading and culminating in a generalised tonic-clonic seizure). Some provoking factors for seizures might initially seem just too bizarre to be true: eating, tooth brushing, hot water (especially as a genetic trait in India), micturition, and emotionally triggered seizures.14 Sexual activity may rarely triggers epileptic seizures (orgasmic epilepsy): case reports suggest that this occurs mainly in women and mostly localises to the right hemisphere on inter-ictal EEG. Startle-induced epilepsy is rare (considered under Borderland of epilepsy section), and manifests as seizures provoked by startle phenomena in genetically susceptible children.
Seizures where mimics are more likely
Special situations
Loss of consciousness in certain situations may imply diagnoses other than epilepsy.
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Seizures in the bathroom, a restaurant, and the doctors’ surgery, prompt the likely diagnosis of syncope (provoked by posture, heat, sight of blood, etc).
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Seizures on a psychiatric ward or in patients with strong psychiatric history prompt initial suspicion of psychogenic non-epileptic attacks.
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Seizures on a cardiac ward may be understandably suspected first as having had cardiac syncope.
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Seizures on an intensive care unit may sometimes be first attributed to movement disorder associated with either metabolic disturbance or hypoxic-ischaemic encephalopathy.
Seizures accompanying existing conditions
Some clinical situations are so dominated by associated features that epileptic seizures can be overlooked.
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Psychiatric history: Seizures in a person with chronic anxiety, self-harm, drug addiction, dyscontrol (eg, following previous head injury) risk, despite their increased risk of epilepsy, being labelled as psychogenic episodes.
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Learning disability: Seizures, particularly of complex partial (dyscognitive) type in someone with significant intellectual disability, may easily be labelled as a behavioural disturbance only.
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Neurodegenerative disease: Seizures in patients with Alzheimer's disease or Huntington's disease (eg, blank spells or automatism) may be ascribed to movement disorder or behaviour disturbance.
Spontaneous seizures where acute symptomatic seizures are more likely
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Diabetes mellitus, with previous hypoglycaemic episodes, may lead to subsequent sleep-related seizures being too easily attributed to hypoglycaemia. This mislabelling sometimes persists despite documented normal ictal plasma glucose levels.
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Alcoholism, with previous alcohol withdrawal seizures, may delay the diagnosis (and management of) epilepsy, with seizures being presumed due to alcohol withdrawal.
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Illicit drug use, for example of cocaine or intravenous drugs, may prompt the clinician to think first of psychogenic non-epileptic seizures or drug withdrawal seizures, rather than epilepsy.
Seizures in rare conditions
Some rarely encountered conditions may present with seizures but, because of other manifestations, the seizures may be mislabelled and the underlying condition remain undiagnosed.
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Autoimmune encephalitis: The facio-brachial dystonic seizures characteristically preceding limbic encephalitis due to voltage-gated potassium channel-complex-antibody (VGKC-complex-Ab) manifest as brief (a few seconds) and frequent (eg, 50 per day) dystonic seizures, easily be mislabelled in the context of behavioural disturbance and memory loss, especially as they are typically resistant to antiepileptic medication (though responsive to immunosuppression).15
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Acute intermittent porphyria: Patients with seizures caused by porphyria may have these mislabelled as psychogenic non-epileptic seizures—understandable, given their psychiatric manifestations and paradoxical worsening of symptoms on taking antiepileptic medications such as carbamazepine.
Where the tests do not help and even hinder
The gold standard for diagnosing epilepsy is to record a seizure with video EEG. Again, the stereotyped nature of seizures (perhaps more that for other types of event) may be a big pointer to their diagnosis. Even here, however, some seizures may escape diagnosis.
Normal EEG during seizures
Brief seizures arising from a deep midline focus may not be detected on a surface EEG, especially if there is a lot of movement artefact (see above, especially frontal and parietal seizures).
Abnormal EEG obscuring seizures
Seizures occurring in conditions where the EEG is already very abnormal, for example, acute viral encephalitis or Creutzfeldt–Jakob disease, may be overlooked on the EEG recording.
Conclusion
Many conditions mimic epileptic seizures (especially syncope and psychogenic non-epileptic seizures), giving a well-known risk of misdiagnosing and unnecessarily treating epilepsy where it does not exist. The converse, where the underlying cause is epilepsy but it is overlooked or misdiagnosed as something else (epilepsy chameleon), is less of a problem that often needs clarifying. A further group of conditions lie at the borderland between epilepsy and ‘not epilepsy’, the so-called borderland of epilepsy, where better understanding of the pathophysiolgy will eventually clarify the cause.
References
Footnotes
This paper was reviewed by Mark Manford, Cambridge, UK.
Competing interests None.
Provenance and peer review Commissioned: externally peer-reviewed.
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