Everyday activities that occur during sleep w/o knowledge of doing so. SW occurs during NREM early in the night and may act as if awake but speech is nonsensical. They have no recollection and serious injury can entail. Most prevalent in children and boys. Adults who SW have increased prevalence of anxiety disorders & PDs Genetic – family studies show 10x more prevalence in 1st degree relatives + twin studies showing 50% cc in MZ. It seems to be a genetic brain abnormality of being woken during SWS but arousal is incomplete.
SWS -Children have increased SWS. Oliviero -the system that normally inhibits motor activity in SWS is not developed in children. Supported by sleep walkers having immaturity in neural circuits involved in motor excitability Factors -psych illnesses, stress, anxiety and some drugs. Longitudinal research from sleep centre showed link between sleep deprivation and walking. Baseline showed 50% SW vs. after deprivation 90% of them did + increase in episodes (only for those w/ predisposition)
Evaluation Sleepwalking starts in childhood when daytime sleeping stops (this contradicts evo) Diathesis-stress model – genetic predisposition + maturity of neural circuits / SWS amount (which is in turn increased by other envi factors such as drugs and alcohol)
Narcolepsy Disorder of sleep/wake cycle. Results in sudden uncontrollable attacks of REM sleep with variance in time. It involves daytime sleepiness and may not realise after microsleep they weren’t awake. The other main symptom is sudden loss of muscular control triggered by strong emotions called cataplexy. Similar to REM, everything is functional but muscle control in body is lost. Other symptoms inc. hallucinations, auto behaviour and interruption of night time sleep marked by craving of sweets and physiological arousal. Usually starts in adolescence
REM – Malfunction of REM due to association of hallucinations and muscle activity loss (cataplexy) HLA – mutation of the immune system where an increase of HLA was found in narcoleptics Hypocretin – Involved in regulating arousal. Dement – mice w/o hypocretin had narcolepsy + deliberate bred dogs w/ faulty hypocretin receptors also did. Levels of hypocretin in spinal fluid were near non-existent in human narcoleptics
Genetics – 25% cc rate. Suggests environment plays a role Evaluation REM theory supported by neuron activity in the brainstem of narcoleptic dogs when cataplexy occurred so did neuron activation only occurred in normal dogs during REM. Is however, a lot of disputes over this theory The specific HLA variant found commonly in population and only minority of narcoleptics