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Patients may be amnesic for events but often describe dream-like experiences such as seeing
spiders, feeling chased, and house/walls collapsing on them. These events are not as narrative
as dreams associated with REM sleep. Events may also be related to daytime frustrations or
incidents. The bed partner may describe fearfulness or confusion and patients may get out of
bed with these events. These conditions are most common in children (up to 20% of children
sleep walk). Symptoms may also occur in adults, up to 2–3% are said to have events at least
once a year. There is often a history of NREM parasomnias in childhood but NREM
parasomnias may also start in adulthood.

The similarities between features seen during NFLE and NREM parasomnias have prompted
the hypothesis that the disorders may have a common pathogenic background27. Central
pattern generators (CPGs) are neuronal networks activating specific sequences of motor
responses. These are usually controlled by the cortex, but temporary loss of this control, either
by sleep or epilepsy, facilitated by arousal, can result in the emergence of stereotyped inborn
fixed action patterns seen in both NFLE and NREM parasomnias27-29. Such ‘release
phenomena’ include oroalimentary automatisms, bruxism, pedalling activity, wanderings,
and emotional responses (ictal fear, sleep terrors)30. There does also appear to be an unusually
high proportion of patients with NFLE reporting a history of parasomnia, up to 34%22. A
recent study also found a higher proportion of relatives with parasomnias in relatives of
patients with frontal lobe epilepsy compared to relatives of normal control subjects31.

Treatment of NREM parasomnias is mainly non-pharmacological, including sleep hygiene
and avoiding triggers. Patients can be reassured that the parasomnias themselves are benign
but safety aspects (such as ensuring doors and windows are properly closed and locked and
that objects with which patients can hurt themselves or partners are locked away) are
important to avoid injury to patient or bed partner. In more severe cases pharmacological
treatment may be indicated. There are no randomised controlled treatment trials of NREM
parasomnias but there are case series reporting efficacy of both long-acting benzodiazepines
(clonazepam) and antidepressants (for example paroxetine or clomipramine).

REM sleep behaviour disorder (RBD)
1. Occurs during second half of night
2. 12 episodes per night (but often smaller movements more frequently during REM
sleep)
3. Frequency varies (but usually most if not every night)
4. Mean age at onset 5055 years.

Normally there is muscle atonia during REM sleep to ensure we do not act out our dreams.
In REM sleep behaviour disorder (RBD) there is loss of this normal atonia during REM sleep.
For a diagnosis of RBD there must also be a history of or observed motor activity during
REM sleep. There will often be vivid dreams with some recall, but patients are usually
unaware of events. Movements are often reported to be violent and may injure the bed
partner. However, during polysomnography, a wide range of movements and behaviours can
be seen and it is possible that it is the violent movements that wake the bed partner up and is
hence reported. Onset is often later in life and in a large proportion of cases (3090%
depending on study and duration of follow-up), RBD is symptomatic of an underlying
neurodegenerative disorder such as dementia, Parkinson’s disease, multiple system atrophy
or cerebrovascular disease32-34. RBD may pre-date the onset neurodegenerative disorder. It
has been suggested that the risk of developing Parkinson’s disease is related to the severity
of loss of REM atonia on polysomnography35. RBD may also be secondary to withdrawal
from alcohol or sedative drugs or precipitated by drugs including tricyclic antidepressants,
SSRIs or other types of antidepressants (mirtazapine). It may also be seen in younger patients
with other sleep disorders such as narcolepsy. In these patients there does not appear to be