Insomnia - the innability to sleep and is extremely widespread.
Symptoms of insomnia
- Decreased alertness
- Poor concentration
- Overly emotional
Diagnostic criteria for insomnia
- Taking longer than 30 mins to sleep
- Being asleep for less than 85% of the time while in bed
- Increased number of night-time awakenings
Secondary Insomnia - problems with the quality and duration of sleep leading to daytime sleepiness which is caused by a pre-existing condition.
- Psychological disorders such as depression, anxiety and schizophrenia. 40% of patients with insomnia have a psychological disorder.
- Physiological disorders such as parkinsons disease, CHD or chronic pain. In addition, the treatments for certain physiological conditions can to lead to insomnia e.g. steriods.
- Sleep related events such as sleep walking and sleepapnea, these are called parasomnias. Sleepapnea is temporary interuptions in breathing, the sufferer wakes up frequently as a result.
- Fatal Familial Insomnia - during middle age the person stops sleeping leading to death within weeks. This is a genetic condition resulting in the gradual degeneration of the part of the brain called the thalamus which controls levels of conciousness.
Explanations and treatments for insomnia
Stimulus control therapy - Based on the recognition that some insomniacs often report having problems sleeping in their own bed but fall asleep quite quickly in front of the TV or in a hotel. Such individuals associate bed time with other activities. SCT involves changing behaviour to break the association between activites which are 'arousing' and bedtime.
- Only going to bed when sleepy
- Not taking naps in the daytime
- Removing media from bedrooms
- Develop a regular bedtime
Cognitive behavioural therapy (CBT) - People who suffer from insomnia often report anxiety before bed. The believe they should go to sleep quickly and sleep for 7-8hrs. The harder they try to sleep the less they will sleep. CBT is aimed at correcting these faulty cognitions. Causes of insomnia are discussed with the client.
Causes of insomnia - conclusions
Stimulus control therapy therefore suggests that insomnia is caused by maladaptive behaviour. This therapy is based on classical conditioning. CC suggests that people associate the bedroom with not sleeping.
CBT suggests that insomnia is caused by faulty thinking which leads to anxiety about their inability to sleep. Thus a visious develops which exacerbrates the problem.
Anxiety is an important issue in inhibiting sleep. It is incompatible with sleep and whether it is due to the sleep problem itself, techniques which reduce arousal are likely to be effective.
The relationship between personality and insomnia
People with anxious personalities are more likely to suffer from insomnia as they have high levels on physiological arousal (heart rate etc) which acts again the tendency to sleep. This is supported by CBT as it reduces anxiety making it an effective treatment and twin studies have shown there is a high concordance rate for insomnia.
Neuroticism - a personality type characterised by high levels of anxiety and bodily arousal.
Chronotype - a personality type defined by our sleep wake patterms.
Extreme larks (alert early) and extreme owls (alert late at night) cannot fit into the 9-5 culture as they are both extremes of sleep. So if you wake up earlier you will fall asleep earlier and vice versa.
Evaluation of insomnia
There are many different types of insomnia each with a different cause that it is nearly impossible to make generalisations that will describe all cases of insomnia in a meaningful way
Dement (1999) states that insomnia is not a sleep disorder at all but a symptm of other illnesses e.g Parkinsons disease. This is an important issue for treatment as how we view insomnia eith as a symptom or a condition on its own will lead doctors to offer very different treatments.
The cognitive approach highlights the problems of using the subjective self reports of people who claim to have insomnia. Some people believe that they have insomnia because they are not getting 8 hours sleep. However such individuals may not have insomnia at all but their bodies need less sleep than average.
A more valid method than self reports may be lab based research studies using EEG to measure patterns of sleep. Some researchers have questioned the use of EEG as the sole basis for determining if someone is asleep. A number of studies have shown discrepancies betwen behavioural and EEG sleep criteria. This highlights the problem of taking a reductionist approach in the study of sleep.
Sleepwalking - a condition which occurs during sleep when an individual leaves their bed and walks around as if awake.
Sleepwalking is more common in childhood and affects boys in particular. They tend to be hard to wake and even though their eyes are open, they usually appear dazed.
Explanations for sleepwalking
Sleepwalking usually occurs during deep, non-REM sleep.
Oliviero (2008) believes that sleep disorders such as sleepwalking arise when normal physiological systems are active at inappropriate times. During sleep the parts of the brain which control the movement of muscles are suppressed by other parts of the brain. In individuals who are susceptible to sleepwalking this suppression may be incomplete because of genetic or environmental factors or physical immaturity.
Zadra et al (2008) Sleep dep and sleepwalking
Zadra investigated the link between sleep deprivation and sleepwalking. 40 suspected sleepwalkers were admitted. First, they measured their baseline sleep patterns. During a subsequent visit they were kept awake for 25hrs. Ps were evaluated on a three point scale based of the complexity of their actions.
Results - normal sleep: half of the Ps showed 32 sleep walking behaviours
- recovery sleep: 90% of P's showed 92 sleep walking behaviours.
Conclusion - Sleep deprivation increases the amount of sleep walking
Evaluation of sleep walking
There is strong evidence that sleepwalking is genetic. Broughton (1968) found that the prevalence of sleepwalking in first degrees relatives of an affected subject is at least 10 times greater than in the general population.
Lecendreux et al (2003) report about a 50% concordance rate in MZ twins compared to 10-15% in DZ twins and also have identified a gene which may be critical in sleep walking.
In the Zadra study sample sizes were relatively small and there still exists the possibility that sleep behaviours in the lab are different from that experienced at home. Lab studies create an artifical environment and P's may not sleep as they normally would.
Some researchers question the use of EEG as the sole basis for determining if someone is alseep and therefore if their sleepwalking behaviour is occuring during sleep.
Basetti (2002) discovered a biological explanation for sleepwalking. He studied 74 patients who were diagnosed with adult sleepwalking an found that of the 16 patients who had genetic testing, 50% of them had a specific gene that was present in only 24% of healthy people.
Narcolepsy - a sleep disorder which leaves the sufferer with an innabilty to stay awake during the day.
There are four general symptoms (only 50% of sufferers show all four symptoms):
- Severe daytime sleepiness - narcolaptics have an ongoing struggle to stay awake which interferes with daytime activities.
- Cataplexy - which the skeletal muscles suddenly relax causing the person to collapse. The person remains concious.
- Sleep paralysis - when a person is paralysed when falling asleep or just on waking but the person feels awake.
- Hypnogogic hallucinations - dream like experiences whilst still awake.
Explanations for narcolepsy
People with narcolepsy do not follow the same stages of sleep as non-sufferers. It has been found that narcoleptics REM sleep occurs at inappropriate times in sufferers and this can account for one of the symptoms of narcolepsy - hypnagogic hallucinations.
Much has been learned for dogs susceptible to narcolepsy. As a result a gene defect has been identified which plays a role in narcolepsy. The gene is responsible for regulative brain receptors for the neurotransmitter called Orexin. Without receptors Orexin cannot function and it was proposed that lack of Orexin in the brain was the cause of narcolepsy in humans.
Therefore it would appear that there is evidence of a biological basis for narcolepsy. However twin studies have shown that while MZ twins have a higher concordance rate than DZ twins, the concordance rate for MZ twins is only around 30%, suggesting the condition is not entirely inherited.
Drugs which correct levels of Orexin aren ot yet available but stimulants such as Ritalin and amphetamines appear to alleviate symptoms as they combat the daytime sleepiness.
Evaluation of narcolepsy
It is clear that there is a genetic component ot narcolepsy. In dogs it is clear from research that one gene can pass on the trait, whereas in humans it does not. In humans there is only a 30% concordance rate in MZ twins. This raises questions about the relevance of animal studies to investigate human behaviour. There are also ethical issues raised by breeding animals with a condition which may affect the quality of their lives.
It is clear that Orexin plays an important role. The absence of Orexin has not been found in any other conditions suggesting that determination of the absence of Orexin in cerebro-spinal fluid is a good measure for diagnosis. This highlights the advantage of taking a reductionist approach to studying human behaviour. This approach has allowed psychologists to draw conclusions about patterns of cause and effect in this case.
As yet there are no Orexin replacement treatments available although stimulant drugs appear to relieve the symptoms.