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occur from sleep, and may occur in clusters of 56 or more per night, usually with partial
recovery between, but status epilepticus is also common.

Seizure manifestations2,47,9. The seizure semiology is dependent on the area of cortex
activated during a seizure, and therefore can give important clues as to the presumed
epileptogenic zone. However, the area of cortex generating symptoms during seizures need
not be identical with the epileptogenic zone, as spread frequently occurs from the area of ictal
onset. Understanding the functional anatomy of the frontal lobes allows us to link clinical
symptoms during the seizure and areas of cortex activated, and electro-clinical characteristics
have been recently summarised19-21. For practical purposes in epileptology the main areas of
the frontal lobe are defined by stimulation and lesion studies and include:

The primary motor areas (precentral gyrus); supplementary sensorimotor areas (SSMA) in
the mesial aspect, the posterior part of the superior frontal gyrus and in the paracentral lobule;
the frontal eye field in the posterior part of the middle frontal gyrus; the frontal language area
in the pars opercularis and triangularis in the dominant inferior frontal gyrus; the prefrontal
cortex; and the orbitofrontal cortex. Negative motor areas are represented in the posterior
inferior frontal gyrus and in the posterior mesial superior frontal gyrus in front of the SSMA
proper.

Frontal lobe seizure semiology with predominantly positive motor symptoms can be grouped
into three main categories: 1) focal clonic seizures; 2) bilateral asymmetrical tonic seizures;
3) complex motor seizures; 4) other rarer seizure semiologies as listed below.

1) Classical, hemiclonic Jacksonian motor seizures are the easiest to localise, invariably
involving the contralateral motor strip. Consciousness is usually preserved. There may
be a short preceding aura (non-specific or sometimes somatosensory, the latter likely in
part due to some overlap of motor and sensory representations in the pericentral region).

2) More anteriorly, in the supplementary motor area (SMA) medially and the premotor
cortex (PMC) laterally, more complex motor manifestations are recognised: turning of
head and eyes and posturing of arms and legs. Classically, SMA seizures cause sudden
assumption of a ‘fencing posture’, the contralateral arm being abducted at the shoulder,
externally rotated, flexed at the elbow. Though characteristic, these seizures are not
pathognomonic of SMA, or even frontal, onset. Motor automatisms may occur,
particularly in PMC seizures, although it is not entirely clear whether this is partly due
to temporal lobe involvement. The seizure may be preceded by a vague somatosensory
aura such as numbness or tingling, more poorly localised than in parietal seizures.
Vocalisation at the onset of the seizure is also common. These motor manifestations may
be ipsilateral, contralateral or bilateral from a unilateral discharge. Consciousness may
be retained. Secondary generalisation may be too rapid for the posturing to be detected.

3) Complex motor seizures. Such seizures may arise from frontopolar, anterior cingulate,
opercular-insular and orbitofrontal regions. There is usually complex motor activity,
usually considered ‘hypermotor’, ‘gestural’ or ‘repetitive’. There may be somatic,
experiential or psychic aura, and so these may cause confusion with temporal lobe
seizures; there may be an aura including epigastric sensations and olfactory
hallucination. Autonomic manifestations are common, e.g. facial flushing and/or pallor,
tachycardia, pupillary dilatation and incontinence of urine. Speech arrest may be seen,
particularly in dominant hemisphere seizures, and there may be a post-ictal phase of
predominantly expressive dysphasia. Spread of the seizure discharge posteriorly may
produce PMC and SMA manifestations. Motor automatisms are common.