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Night Fears

Night Fears (NS) or Nocturnus is a paroxysmal nonepileptic disorder that occurs during the phase of slow sleep and manifests itself as a complex of psychomotor and vegetative disorders with subsequent amnesia. Nightmares, unlike night terrors, appear in the phase of REM – sleep, manifested by frightening dreams and do not amnesia. According to the modern classification of sleep disorders, night terrors belong to the group of parasomnia or awakening disorders from the slow wave sleep phase. Parasomnia also includes sleeping, night cluster headache, chronic night paroxysmal hemicrania, night yaktation (jactacio capitis nocturna). The concept of parasomnia was introduced by Gastaut & Broughton in 1965. The authors have identified 3 most important features typical for this group of diseases:

Night Fears
  • paroxysmal onset soon after falling asleep,
  • sleep interruption,
  • occurrence exclusively in the phase of slow wave sleep.

Subsequent studies using video – EEG – monitoring and polysomnography have proven the non-epileptic nature of parasomnias and their lack of association with epilepsy.

In the etiology of night fears, the hereditary factor is recognized as the leading one. Autosomal dominant inheritance with incomplete penetration is assumed. Among relatives of proband who suffer from night fears, cases of various forms of parasomnia are often found, mainly dreams. Some authors in the emergence of night fears pay attention to exogenous factors, in particular, the presence of a chronic psychotraumatic situation. Psychological testing of children suffering from night fears rarely reveals an increased level of anxiety and aggressiveness.

The prevalence of night fears is not precisely known. Most studies report a frequency between 1 and 3% among a population of children between 1 and 14 years of age.


Night Fears

The disease begins in childhood in a wide age range from several months to 15 years. With a maximum frequency night fears debut at the age of 5 – 7 years, with some predominance of boys. Clinical manifestations of night fears are typical and stereotypical. The triad of symptom complexes is typical: mental, motor and vegetative. A child’s sleep is suddenly interrupted by a scream, usually 30 – 60 minutes after falling asleep. He sits in bed; on his face – a grimace of fear. It is possible psychomotor excitement, chill-like hyperkinesis, visual hallucinations of frightening content. When the mother tries to calm down, hug or tuck the child, the patient does not recognize her and repels her. It is not possible to get in touch with the child. There are vegetative disorders: tachycardia, tachypnea, mydriasis. The duration of the attack varies from 30 seconds to 10 – 15 minutes, averaging 2 – 5 minutes. After the seizure or when you wake up in the morning, these conditions are amnestied. The frequency of attacks is extremely variable from several paroxysms during one night to single ones during the whole period of the disease. In general, the NS is characterized by a high frequency of seizures.

During routine neurological examination, no pathology is revealed, and the intellect is always preserved. Neurotic features of personality development are often stated.

Video EEG monitoring and polysomnographic examination are of the most important importance in the diagnostics of night fears. The EEG study does not detect epileptic activity, neither in the interictal period, nor during an attack. In polysomnography, the occurrence of paroxysms is clearly visible only in the phase of slow sleep, usually in stages 3-4. During night fears, a generalized symmetrical hypersynchronous delta activity may be detected on the EEG, which differs from the slowwave sleep patterns. Some authors note sleep disturbance in night fears (especially in the first 30-60 minutes after falling asleep): Slow wave phase shortening and REM sleep lengthening. Differential diagnosis should be made with other parasomnias and with partial forms of epilepsy. During complex partial epileptic paroxysms, the effect of fear is less pronounced and motor symptomatology prevails. On the EEG, a regional peak – wave activity, usually in frontal or temporal drainage – is often observed.