Epilepsy Figure 2: In What Sleep Stage do Seizures Occur? 100
lacks a narrative structure and consists of escaping from something or someone. Confusional arousals consist of episodes of confusion arising from sleep, about which the person is usually amnesic.
75 50 25 0 Light sleep Deep sleep REM
The majority occur during light sleep (proportionate to the amount of light sleep in a night). Seizures rarely occur during rapid eye movement (REM) sleep. Source: Sinha et al., 2006.9
Figure 3: Scheme for Differentiating Non-rapid Eye Movement Parasomnia from Nocturnal Frontal Lobe Epilepsy
Is there a discrete offset to the event (as opposed to a gradual emergence of full
consciousness)?
Does the patient clearly arouse fully (i.e. to normal
wakefulness) at the end of the episode?
Is there versive head turning ± dystonic posturing during the event?
NFLE NFLE
Does the patient remain prone/ supine, (i.e. does not sit, stand or walk during the episode)?
NFLE
NREM parasomnias and epilepsy can sometimes be difficult to distinguish, especially on history alone. Furthermore, they can co-exist in the same subject. There is an unusually high proportion of patients with NFLE reporting a history of parasomnias – 34% in one survey.35 This could tentatively be due to nocturnal epileptic seizures erroneously being diagnosed as parasomnias in childhood and only when episodes continue later in life being correctly diagnosed as epileptic seizures, or it could be the precipitation of NREM parasomnias by disruption of sleep by seizures. However, a recent study has confirmed an increased frequency of arousal parasomnias in families with NFLE compared with control subjects, supporting the hypothesis that there could be a link between the two involving abnormal arousal systems.37
The similarities between features seen during NFLE and parasomnias have prompted the hypothesis that the disorders may have a common pathogenic background.38
the triune brain: neomammalian brain (neocortex), paleomammalian brain (limbic system) and reptilian brain (basal ganglia).39
Normally,
central pattern generators (CPGs), neuronal networks activating specific sequences of motor responses in the paleomammalian and reptilian brain, are controlled by the neomammalian brain. However, sleep or epilepsy remove this control (inhibiting the neocortex) and, facilitated by arousal, this results in the emergence of stereotyped inborn fixed action patterns.38
Parasomnia
oroalimentary automatisms, bruxism, pedalling activity, wanderings and emotional responses (ictal fear, sleep terrors).40
In support of this Parasomnia Yes No
NFLE = nocturnal frontal lobe epilepsy. Source: Derry et al., 2009.41
arousals, sleep usually lightens after epileptic arousals, while people often return to the same sleep stage with brief physiological arousals/movements. Seizures cluster and occur throughout the night, often many times per night.
NREM parasomnias usually occur from deep sleep.36 There are three
NREM parasomnia can be precipitated by sleep deprivation, stress and other sleep disorders (e.g. sleep apnoea). People are invariably confused during the event, and are usually amnesic for the event. These conditions are most common in children, but do occur in adults. They occur usually one to three times per night and mostly in the first third of the night (when deep sleep is occurring).36
main subtypes of NREM parasomnia: sleepwalking (somnambulism), night terrors (pavor nocturnis) and confusional arousal. Certain people seem predisposed to having NREM parasomnia and there is often a family history.36
Sleepwalking is characterised by wanderings, often with associated complex behaviours such as carrying objects and eating. The episode usually lasts a matter of minutes. Night terrors are characterised by screaming and prominent sympathetic nervous system activity (tachycardia, mydriasis and excessive sweating). If woken from these, people will often recall dream mentation that usually
62
theory is the observation that minor motor events associated with frontal lobe epilepsy are often not directly associated with epileptiform discharges, raising the possibility that their genesis is due to the non-specific triggering of CPGs by either epileptiform discharges or fluctuations in arousal, or even that epileptiform discharges induce minor motor events by provoking an arousal.38,40 Indeed, a seizure discharge could act as an internal arousal stimulus and its effect would therefore be similar to that of an intrinsic (snore, cough) or extrinsic (noise) physiological stimulus. This results in non-specific arousal behaviour that does not depend on the nature of the stimulus.41
Is there any way of clearly distinguishing nocturnal frontal lobe seizures from parasomnias? If they are very brief, it can be particularly difficult. However, distinguishing on the basis of frequency, time of night and stage of sleep can be particularly useful. Furthermore, there are semiological features that can help distinguish the two.41 Importantly, brevity, sitting, standing/walking, preceding arousal or fearful emotional behaviour are not good differentiators. Stereotypy and dystonic posturing are more common features in seizures, while yawning, waxing and waning, prolonged duration (over two minutes) and indistinct offset are more common in parasomnias.41
This last
feature is quite a notable difference between seizures and NREM parasomnias on video. A scheme has been devised by Derry and co-workers that can differentiate the majority of seizures and parasomnia (see Figure 3).41
Nevertheless, even with access to
good-quality video-EEG telemetry, the differentiation can be difficult and there is often disagreement between experts who are shown the same videos.42
EUROPEAN NEUROLOGICAL REVIEW
This builds on MacLean’s idea of
Such release phenomena include
Percentage (%)
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