Unable to sleep due to situational factors may occur because the individual is feeling stressed or depressed but such psychological states are not the problem – it is the insomnia that is the problem, insomnia= unidentifiable causes, which disappear but the insomnia still remains.
Or… single medical, environmental or psychiatric = underlying the problem. In such cases insomnia is a symptom of a main disorder, which is why it’s secondary. Like to occur in people who do shift work or who have circadian rhythm disorders, such as delayed sleep phase disorder.
Use of stimulants. Even though caffeine near bedtime may not disturb sleep, it may trigger awakenings later. Caffeine related ingredients are also found in soft drinks, chocolate, and strong tea. Nicotine is a stimulant and it has been shown that smokers take longer to fall asleep and sleep worse than non-smokers. other factors= Noise, light, irregular sleeping hours that frequently change in sleep time, an inactive lifestyle, failing to shift into full and active wakefulness during the day usually fails to shift into a deep sleep at night e.g ageing people, stress- exams, pain is also a reason for insomnia, disorders such as arthritis, back injury, headache and many other forms of discomfort may also upset sleep
Speilman and Glovinsky (1991) distinguished between predisposing precipitating and perpetuating components. Predisposing factors include a genetic vulnerability e.g. twin studies indicate that 50% of the variance in the risk insomnia could be attributed to genetic factors.
Watson et al (2006) research suggests that physiological factors may predispose a person to develop insomnia. However predisposing factors alone are unlikely to explain chronic primary insomnia, the diathesis-stress model of mental disorders proposes that environmental stressors are needed to precipitate the disorder. In the case of insomnia, stress or environmental changes may trigger episodes of insomnia.
Ohayon and Roth (2003) found that insomnia may not be just an effect of an underlying disorder. A study was done on 15,000 Europeans and it was shown that insomnia followed cases of mood disorder. Therefore, it’s the insomnia that causes mood swings and not the other way around. This study is high in population validity, making it more generalisable. A weakness is, however, that it has a cultural bias towards Europe and is less representative of other cultures and the extent to which it can be applied universally is reduced.
Hublin et al, (1997) Sleep walking is a disorder which is most common in childhood, affecting about 20% of children and less than 3% of adults. SW occurs only during non REM/SWS sleep and is related to night terrors which is also only found in NRM sleep.
Incomplete arousal: EEG recordings made during Sleepwalking show a mixture of the delta waves which are typical of SWS (slow wave sleep) plus the higher frequency beta waves which are characteristics of the awake state.
It looks as if Sleep waking occurs when a person in deep sleep is awakened by the arousal of the brain is incomplete. It is likely this this abnormal arousal is GENETIC.
One possibility is that it happens because children have more SWS than adults.
Oliviero (2008) suggested that the GABA system that normally inhibits motor activity in SWS is not sufficiently develop in some children, and it is also may be undeveloped in some adults. Insufficient amounts of GABA leave the motor neurons capable of commanding the body to move even during sleep. Found that adult sleepwalkers had signs of immaturity in the relevant neural circuits when compared with normal controls.
Broughton, (1968) found the prevalence of sleepwalking in first degree relative of an affected subject it atleast ten times greater than in the general population - reductionist- ignores enviro.
Also twin studies have been used, Lacendreux et al (2003) = 50% concordance rate in MZ twins compared to 10-15% in DZ twins. He also identified a gene which may be critical in sleepwalking as well as night terrors. reliability not 100% other factors? reductionist- ignores enviro.
factors cause SW=Sleep deprivation Fatigue Stress Anxiety Fever Sleeping in unfamiliar surroundings Some medications, such as zolpidem (Ambien, Edluar)
The diathesis-stress model (vulnerability) comes from a genetic predisposition for the disorder. Strong evidence that SW = genetic basis. The stress part of the diathesis-stress model might be represented by environmental factors; frequent nightly awakenings.
Narcolepsy is a disabling disorder of sleep regulation that affects tge control of wake and sleep. It may be described as an intrusion of dream sleep (REM) into the waking state. Symptoms generally begin between the ages of 15 and 30.
The four classic symptoms of the disorder are, excessive daytime sleepiness, cataplexy (sudden, brief episodes of muscle weakness or paralysis brought on by strong emotions such as laughter, anger, surprise or anticipation), sleep paralysis, hypnagogic hallucination (vivid dreamlike images that occur at sleep onset).
Thanickal et al (2000) due to mutation of the gene which codes for receptors for the neurotransmitter, hypocretin (or Orexin). Hypocretin receptors are found in the hypothamalus(sleep centre) which is thought to be involved in wakefullness. Showed that there is an 85-95% reduction of hypocretin receptors in narcoleptic humans (AO2- scientific measurement; PET SCANS). 4 narcoleptic brains compared to 12 normal brains. (AO2 - Small sample, Scientific measurement of brain structure by scanning, Qualitative data= can analyse easily.)
Guilleminault et al (1989) – First degree relatives have a 40 fold chance of inheriting narcolepsy. AO2- deterministic – Narcolepsy is predetermined, cannot be address.
Contradicting: Mignot (1998) MZ twins where one has narcolepsy, the second is only effected 25% of the time, thus makinng the genetic explanation reductionist
Honda and Matsuki (1990) – environmentally influenced, not just genetic. Used canine dogs (anthropomorphic). Scientific measurement of brain structure, found the mutation of the gene that codes for hypocretin receptor in the hypothamaus.
AO2 - The breeding of dogs in order to study NARCOLEPSY –ethical? Generalisable?
Additional info on HYPOSOMNIA
Hypersomnia is a disorder characterized by excessive amounts of sleepiness. There are two main categories of hypersomnia: primary hypersomnia (also called idiopathic hypersomnia) and recurrent hypersomnia (also called primary recurrent hypersomnia). Both have the same symptoms but differ in how often they occur
Those who suffer from hypersomnia have recurring episodes of excessive daytime sleepiness (EDS) which is different from feeling tired due to lack of or interrupted sleep at night. They are compelled to nap repeatedly during the day, often at inappropriate times such as at work, during a meal, or in conversation. These daytime naps usually provide no relief from symptoms. Recurrent hypersomnia is characterized by recurring periods of symptoms many times throughout the year mixed with periods of normal sleep-wake cycles.
Kleine-Levin syndrome is the most well-known form of recurrent hypersomnia, though it is very rare, these people often sleep up to eighteen hours a day and yet do not feel refreshed upon waking.
Additional info on HYPOSOMNIA
People who are overweight may be more likely to suffer from hypersomnia. Although studies have shown a correlation between a lack of sleep and weight gain, sleeping at the level of a hypersomniac can also lead to considerable weight gain. This is because excessive sleeping decreases metabolic energy consumption, making weight loss more difficult. It is also the case that sleep disorders of this nature provoke or initiate weight gain due to a tendency to attempt to manage low energy levels by eating non-complex carbohydrates.
Another possible cause is an infection of mononucleosis, as several instances of hypersomnia have been found to arise immediately after such an infection. It can also be caused in children by influenza.
Excessive daytime sleepiness can be a result of sub clinical hypothyroidism
When the cause of the hypersomnia cannot be determined, it is considered to be idiopathic hypersomnia. Hypersomnia is an uncommon disorder, less than 5% of adults complain of EDS.