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favours an epileptic basis. Non-epileptic seizures show more fluctuation in the level of motor
activity. Some qualitative differences in the movements have been suggested but these are
less clear-cut10.

Frontal lobe seizures versus parasomnias

Paroxysmal motor disorders occurring from sleep include not only frontal lobe seizures, but
also parasomnias. There are benign, unpleasant or undesirable behavioural or experiential
phenomena that occur predominantly or exclusively during sleep. To a reasonable degree
parasomnias, such as sleep-walking or sleep tremors, can be distinguished from frontal lobe
seizures by clinical inquiry. Events in parasomnias tend to last longer individually, are less
likely to occur in clusters in a given night, are more likely to cause complex behaviours, such
as wandering outside the bedroom, and tend to be less stereotyped than frontal lobe seizures.
Prolonged EEG with videopolysomnography may be required to distinguish parasomnias
from frontal lobe seizures. A clinical scale has recently been validated and may obviate the
need for prolonged monitoring in some cases11.

Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE)

ADNFLE is a distinctive disorder, with autosomal dominant (Mendelian) inheritance12. A
number of families have been described across the world. The seizure pattern is remarkably
consistent, with predominantly nocturnal clusters of brief motor seizures, which may be
complex or even violent. Though the semiology may vary between members of the same
kindred, seizures are stereotyped within a given individual. Consciousness may be retained.
Neuroimaging is normal, as may be the inter-ictal and even ictal EEG. Videosomnography
differentiates the condition from parasomnias. Mutations in the neuronal nicotinic
acetylcholine receptor alpha-4 and beta-2 subunits (CHRNA4 and CHRNB2) have been
identified12,13. However, these genes are not mutated in the majority of kindreds, suggesting
genetic heterogeneity despite the clinical homogeneity (see also Chapter 5). Carbamazepine
is usually effective treatment.

Treatment

The pharmacological treatment of FLE is as for other focal epilepsies. There are no good
comparative drug trials specific to FLE. Surgery is less successful than for TLE with
complete remission after focal resection in only 2040%, even in the most highly selected
cases3, though some newer reports document better outcomes14. Seizure freedom rates decline
over the years. A recent large series has analysed 70 patients who underwent a frontal
lobectomy between 1995 and 2003. A favourable outcome was defined as complete seizure
freedom, allowing for auras and seizures restricted to the first post-operative week. The
estimated probability of complete seizure freedom was 55.7% at the first postoperative year,
45.1% at three years after surgery, and 30.1% at five years15. It should be noted that, in
addition to patients becoming seizure free, a significant percentage of patients experience an
80% or more reduction in their seizures. Another recently published cohort of frontal lobe
surgeries documented 55% seizure freedom rate at seven years after surgery16. Completeness
of resection of a visible lesion remains one of the most important predictors of good outcome.
Surgery need not be associated with increased neurological or neuropsychological deficit.
Corpus callosum section may be of benefit in patients with drop attacks, who are at risk of
major injury. This may prevent secondary generalisation, or at least slow seizure spread, with
less devastating collapses17.

Other treatment options for refractory frontal lobe epilepsies include vagal nerve stimulation,
regarded mainly as palliative treatment when focal resective surgery is not possible, and,
more experimentally, repetitive transcranial magnetic stimulation (rTMS)18.