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Attacks of migraine and of epilepsy also have various precipitants in common, such as
hormonal factors and sleep disturbance56. A migrainous aura may have visual, sensory or
motor features that may be suggestive of seizure activity and alertness may be impaired.
There are, however, a number of important semiological differences. Visual migraine auras
are monochromatic, angulated, bright and frequently scintillating. They commence in the
centre of the visual field and gradually evolve over several minutes towards the periphery of
one hemi-field, often leaving a scotoma. They usually last between 30 and 60 minutes. In
contrast, simple partial seizures arising from the occipital lobe are circular, amorphous,
multicoloured obscurations that develop rapidly within seconds, and are brief in duration (23
minutes). They often appear in the periphery of a temporal visual hemi-field, becoming larger
and multiplying in the course of the seizure, while frequently moving horizontally towards
the other side69,70.

Somatosensory migraine commences with unilateral paraesthesias spreading from one area
to another over 1530 minutes, often resolving in the first area before becoming evident in
the next. Epileptic sensory symptoms arise quickly and spread rapidly over seconds to involve
other somatic areas in summation, often culminating in secondary generalisation. Peripheral
neuropathies or radiculopathies also cause sensory symptoms and may be transient if, for
example, they are compressive or inflammatory in aetiology. Neurological examination may
reveal evidence of a fixed neurological deficit, and the circumstances in which the sensory
symptoms develop and lack of associated epileptic semiology rarely result in diagnostic
confusion.

Transient ischaemic attacks (TIAs) are broadly distinguished from seizures and migraine by
their ‘negative’ symptoms, that is, sensory loss, weakness or visual impairment, with retained
awareness. However, tingling and focal jerking may occur in association with local cerebral
hypoperfusion and occasionally with severe bilateral carotid stenosis71.

Vertigo with brief episodes of disequilibrium is often misinterpreted as seizure activity. More
commonly, the symptoms are due to disorders of the peripheral vestibular system, such as
benign paroxysmal positional vertigo or Ménière’s disease. Vertigo may occur as a feature
of focal seizures, arising from the frontal or parietal regions and specifically the intraparietal
sulcus, posterior superior temporal lobe, and the temporo-parietal border regions72-75. Vertigo
observed in epileptic seizures rarely occurs in isolation and other clinical manifestations of
seizure activity, such as impaired awareness, are also usually present. Vertigo due to a
peripheral vestibular disorder is often accompanied by nausea and vomiting and precipitated
by head movement, such as rolling over in bed or on provocation with Hallpike’s manoeuvre.
Focal onset or generalised epileptic seizures may be provoked by the same manoeuvres in
patients with ‘vestibular epilepsy’, a subtype of the reflex epilepsies.

Psychic experiences

Focal seizures arising from the temporal lobe commonly involve psychic phenomena,
including déjà vu, panic and fear, visual, olfactory or auditory hallucinations. Perception of
the environment may be altered with derealisation, micropsia and macropsia, and interaction
with others may be impaired by abnormal language function and altered thought patterns,
seen most commonly in temporal and frontal lobe seizures. Panic attacks, which have a
psychological rather than epileptic basis, are associated with feelings of fear and anxiety,
hyperventilation and palpitations. The diagnosis is usually clear as they are commonly
situational rather than spontaneous, and have a protracted time course with a characteristic
evolution. Simple partial seizures arising from the amygdala can, however, be difficult to
differentiate from brief episodes of fear and anxiety76,77.