Sleeping disorders

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Short term insomnia

Lasts a few days or weeks

Tends to be caused by immediate worries such as:

  • Exams
  • Death in the family
  • Jet lag
  • Noise at night
  • Temporary medical condition such as a cold
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Long term (chronic) insomnia-primary

What is it?

Sleeping difficulties lasting more than four weeks (According to the DSM).

Primary insomnia- Occurs when a person is having sleeping problems that are not directly associated with a health problem or physical cause, such as drug addiction.

  • Feeling depressed or stressed but that is not what causes it.
  • could be due to bad sleeping habits.
  • Insomnia may have a cause but it has disapeared and insomnia persists. This may be because the individual expects the insomnia so continues to cause it.
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Long term (chronic) insomnia- Secondary

This is where the individual is having sleeping problems due to an underlying medical, psychiatric or environmental cause, so is a symptom of something else.

What may cause it:

  • Heart disese
  • Depression
  • Circadian rhthm disorders- eg phase delay syndrome
  • Older people may suffer from rheumatism and less sws so more easily woken
  • Envirnomental factors- tea, coffee, alcohol 
  • Parasomnias such as sleep apnoea, teeth gringing, sleep walking along with many others. 
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Insomnia evaluation

It is important to be able to distingush between primary and secondary insomnia, it can then be treated in the correct way. If it was secondary then it would be no good just to treat a symptom. However Ohayon and Roth (2003) studdied 15,000 European and found that insomnia alone can cause symptoms of depression so may be beneficial to treat it either way.

Consequences of insomnia:

  • Cognitive impairment- Memory loss and poor concentration. Zammit et al (1999) found that insomniacs scored lower on the medical outcomes study cognitive scale than control participants, they demonstrated problems with memory, concentration and problem solving.
  • Accidents- Increase risk of accidents on road. Arendt et al (2001) compared adults who had been deprived of one night sleep to adults who had been given alcohol. They found that even keeping people awake for 3 more hours lead to impairments, equal to a modest level of alcohol. 
  • Psychological disturbance- Insomnia may cause Psychological problems, such as depression and anxiety disorders. Breslau et al (1996) found that insomnia is also associated with increasd risks for drug and alcohol abuse.


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Insomnia evaluation Continued...

  • Immune system underfunctioning- Savard et al (2003) found fewer immune cells in the body with chronic insomnia compared to 'normal' sleepers. This could make insomniacs more vunerable to ilness. however if it is stress causing the sleeping problem then it could be that that also causes low white blood cell count. This highlights an issue with cause and effect.


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Spielman and Glovinsky 1991- Model to explain inso

These people proposed a useful distinction between predisposing, precipitating and perpetuating components to their 3P model of insomnia:

  • Predisposing factors- A genetic vunerability for insomnia. Watson et al (2006) looked at twin studies and concluded that 50% of the varience in the risk of insomnia is genetic. Bonet and Arand 1995, found insomniacs are more likely to experience hyperarousal when both awake and asleep. this would make it harder to sleep and explain why only some people suffer.
  • Precipitating factors- Events that trigger the disorder in vunerble people.Two poeple may experience the same stressors but only one develop insomnia, this is because of predisposing factors. Environmental triggers may be, exams or work etc.
  • Perpetuating factors- Factors that maintain insomnia, even when origional stressors have disappeared or been treated. This could be for example, going to bed tense. 


One of the primary causes of insomnia is the belief that they will not be able to sleep. Storms and Nisbett (1970) treated poeple with a pill and told the individuals it would help them to relax and sleep, acting as a sedative. These patients actually now went to sleep faster because of the placebo affect (the pill was a dummy). 

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Narcolepsy explanations

Narcolepsy is a rare, long-term brain disorder that causes a person to suddenly fall asleep at inappropriate times.

Psychological- Lehrman and Weiss (1943) suggested that sudden attacks of sleepiness disguise sexual fantasies.

REM- In the 1960's and explanation offered for narcolepsy was that is was caused by a malfunction in the system that regulates REM sleep. Evidence to support this is that narcoleptics suffer from cataplexy (loss of muscle tone) and this is the same as what happens during REM sleep. Narcoleptics have disrupted REM sleep during the night but have intrusions of it during the day. 

Human Leukocyte Antigen (HLA) - A mutation in the immune system. Honda (1983) found an increase in one type of HLA in 90% of narcoleptic patients with cataplexy. HLA molecules are found on the surface of WBC's and coordinate the immune response.

Hypocretin-  This is a neurotransmitter recently linked to narcolepsy. Sakurai (2007) found sleep and wake are regulated by interactions of systems that regulate emotion and homeostasis in hypothalamus. Narcoleptics are missing Hypocretin producing cells.

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Evaluation of Narcolepsy

REM- This explanation was supported by Vogel (1960) who found narcoleptics to go straight into REM when falling asleep, where as 'normal' sleepers enter this later in the stages. Sigel (1999) looked at neurone activit in the brainstem of narcoleptic dogs  and it found that cataplexy co-occured with brain cell activity in REM sleep. however other research is not so convincing.

HLA- The HLA variant is not found in all narcoleptics but is also very commin in the general public as well. Suggesting that this cannot be the cause/ only cause. 


  • Evidence of lower levels: Lin et al (1999) found that narcoleptic dogs had a mutation in a gene on chromosome 12 and that this effected the processing of hypocretin. This has been confirmed in human studdies too. 
  • What causes lower levels of hypocretin: In humans it is rarely due to a mutated gene and doesnt seem to be inherited. this is supported by twin studies (Mignot 1998). It seems more likely that low levels are due to brain injury, infection, diet, stress or possibly an auto immune attack. 
  • Linking hypocretin to HLA- Mutaions of HLA affect the immune response, making autoimmune conditions more likely. leading to reduced hypocretin cells (Mignot 2001).
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Sleep walking explanations

Sleep walking is a sleep disorder characterized by walking or other activity while seemingly still asleep. Other names for it are walkingduring sleep and somnambulism.

Incomplete arousal- The brain activity during sleep walking show a mix of delta waves (common in SWS) and beta waves (common in an awake person) this suggests that the person is awakend in deep sleep but the brain arousal is incomplete. In fact it is very diffricult to rouse the person.

Risk factors- Sleep deprivation, alcohol, having a fever, stress or psychiatric conditions tend to increase likelehood of sleep walking (Plazzi et al 2005). Hormonal changes during puberty and menstruation seems to also increase the risk, but only some do it, suggesting it may be inherited.

Why children- 

  • More SWS that adults.
  •  A system that usually inhibits the motor activity in SWS is not developed enough yet and may be under developed in some adults.Olivero 2008 studied the motor excitability of adults while awake and showed to be underdeveloped compared to other adults.
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Evaluation of sleep walking

Genetic basis- Broughton (1968) suggested it may be inherited and found that prevelance of sleep walking in first degree relatives  of an affected subject at least 10 times greater than genral population. Twin studies also support with 50% concordance rate between MZ twins and only 10-15% in DZ twins. There has been a gene that may be critical in sleep walking too. 

Diathesis stress model- genes provide a vunerability (diathesis) but disorder will only appear in situations of environmental 'stress'. Zadra et al 2008 studied 40 patients who were reffered to sleep lab with sleep walking problems. PP's were prevented from falling asleep, on 1st night 50 % of PP's showed signs of sleep walking, which rose to 90% on second night. In this case, sleep deprivation was the stressor. In children SWS acts as the diathesis.

Psychological cause unlikely- One idea is that the individual is acting out dreams, but the fact it occurs in SWS means very unlikely would be related to dreams which occur in REM.

IDA- There have been sleep walking murder situations and the disorder may be used in court.

Hypocretin treatment for narcolepsy isnt an option as the neurotransmitter is broken down before it reaches the brain. The answer may be hypocretin proucing cells transplaned in.

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